" DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."

Saturday, 19 February 2011 02:15

Occupational and Environmental Exposures to the Newborn

Written by
Rate this item
(0 votes)

Environmental hazards pose a special risk for infants and young children. Children are not “little adults”, either in the way they absorb and eliminate chemicals or in their response to toxic exposures. Neonatal exposures may have a greater impact because the body surface area is disproportionately large and metabolic capacity (or the ability to eliminate chemicals) is relatively underdeveloped. At the same time, the potential toxic effects are greater, because the brain, the lungs and the immune system are still developing during the early years of life.

Opportunities for exposure exist at home, in day care facilities and on playgrounds:

  • Young children can absorb environmental agents from the air (by inhalation) or through the skin.
  • Ingestion is a major route of exposure, especially when children begin to exhibit hand-to-mouth activity.
  • Substances on the hair, clothes or hands of the parents can be transferred to the young child.
  • Breast milk is another potential source of exposure for infants, although the potential benefits of nursing far outweigh the potential toxic effects of chemicals in breast milk.

For a number of the health effects discussed in connection with neonatal exposures, it is difficult to distinguish prenatal from postnatal events. Exposures taking lace before birth (through the placenta) can continue to be manifest in early childhood. Both lead and environmental tobacco smoke have been associated with deficits in cognitive development and lung function both before and after birth. In this review, we have attempted to focus on postnatal exposures and their effects on the health of very young children.

Lead and Other Heavy Metals

Among the heavy metals, lead (b) is the most important elemental exposure for humans in both environmental and occupational circumstances. Significant occupational exposures occur in battery manufacture, smelters, soldering, welding, construction and paint removal. parents employed in these industries have long been known to bring dust home on their clothes that can be absorbed by their children. The primary route of absorption by children is through ingestion of lead-contaminated paint chips, dust and water. Respiratory absorption is efficient, and inhalation becomes a significant exposure pathway if an aerosol of lead or alkyl lead is resent (Clement International Corporation 1991).

Lead poisoning can damage virtually every organ system, but current levels of exposure have been associated chiefly with neurological and developmental changes in children. In addition, renal and haematological disease have been observed among both adults and children intensely exposed to lead. Cardiovascular disease as well as reproductive dysfunction are known sequelae of lead exposure among adults. Subclinical renal, cardiovascular and reproductive effects are suspected to arise from lower, chronic lead exposure, and limited data support this idea. Animal data support human findings (Sager and Girard 1994).

In terms of measurable dose, neurological effects range from IQ deficits at low exposures (blood lead = 10 μg/dl) to enceha-loathy (80 μg/dl). Levels of concern in children in 1985 were 25 μg/dl, which was lowered to 10 μg/dl in 1993.

Neonatal exposure, as it resulted from dust brought home by working parents, was described as “fouling the nest” by Chisholm in 1978. Since that time, preventive measures, such as showering and changing clothing before leaving the workplace, have reduced the take-home dust burden. However, occupationally derived lead is still an important potential source of neonatal exposure today. A survey of children in Denmark found that blood lead was approximately twice as high among children of exposed workers than in homes with only non-occupational exposures (Grandjean and Bach 1986). Exposure of children to occupationally derived lead has been documented among electric cable splicers (Rinehart and Yanagisawa 1993) and capacitor manufacturing workers (Kaye, Novotny and Tucker 1987).

Non-occupational sources of environmental lead exposure continue to be a serious hazard to young children. Since the gradual ban of tetraethyl lead as a fuel additive in the United States (in 1978), average blood lead levels in children have declined from 13 to 3 μg/dl (Pirkle et al. 1994). paint chips and paint dust are now the principal cause of childhood lead poisoning in the United States (Roer 1991). For example in one report, younger children (neonates aged less than 11 months) with excessive lead in their blood were at greatest risk of exposure through dust and water while older children (aged 24 months) were at risk more from ingestion of paint chips (ica) (Shannon and Graef 1992). Lead abatement through paint removal has been successful in protecting children from exposure to dust and paint chips (Farfel, Chisholm and Rohde 1994). Ironically, workers engaged in this enterprise have been shown to carry lead dust home on their clothes. In addition, it has been noted that the continuing exposure of young children to lead disproportionately affects economically disadvantaged children (Brody et al. 1994; Goldman and Carra 1994). art of this inequity arises from the poor condition of housing; as early as 1982, it was shown that the extent of deterioration of housing was directly related to blood lead levels in children (Clement International Corporation 1991).

Another potential source of occupationally derived exposure for the neonate is lead in breast milk. Higher levels of lead in breast milk have been linked to both occupational and environmental sources (Ryu, Ziegler and Fomon 1978; Dabeka et al. 1986). The concentrations of lead in milk are small relative to blood (approximately 1/5 to 1/2) (Wolff 1993), but the large volume of breast milk ingested by an infant can add milligram quantities to the body burden. In comparison, there is normally less than 0.03 mg b in the circulating blood of an infant and the usual intake is less than 20 mg per day (Clement International Corporation 1991). Indeed, absorption from breast milk is reflected in the blood lead level of infants (Rabinowitz, Leviton and Needleman 1985; Ryu et al. 1983; Ziegler et al. 1978). It should be noted that normal lead levels in breast milk are not excessive, and lactation contributes an amount similar to that from other sources of infant nutrition. By comparison, a small paint chi could contain more than 10 mg (10,000 mg) of lead.

Developmental decrements in children have been linked with both prenatal and postnatal exposures to lead. prenatal exposure is thought to be responsible for lead-related deficits in mental and behavioural development that have been found in children until the age of two to four years (Landrigan and Cambell 1991; Bellinger et al. 1987). The effects of postnatal lead exposure, such as that experienced by the neonate from occupational sources, may be detected in children from ages two to six and even later. Among these are problem behaviour and lower intelligence (Bellinger et al. 1994). These effects are not confined only to high exposures; they have been observed at relatively low levels, e.g., where blood lead levels are in the range of 10 mg/dl (Needleman and Bellinger 1984).

Mercury (Hg) exposure from the environment may occur as inorganic and organic (mainly methyl) forms. Recent occupational exposures to mercury have been found among workers in thermometer manufacture and in repair of high-voltage equipment containing mercury. Other occupations with potential exposures include painting, dentistry, plumbing and chlorine manufacture (Agency for Toxic Substance and Disease Registry 1992).

prenatal and postnatal mercury poisoning has been well documented among children. Children are more susceptible to effects of methylmercury than adults. This is largely because the developing human central nervous system is so “remarkably sensitive” to methylmercury, an effect also seen at low levels in animals (Clarkson, Nordberg and Sager 1985). Methylmercury exposures in children arise chiefly from ingestion of contaminated fish or from breast milk, while elemental mercury is derived from occupational exposures. Household exposure incidental to occupational exposure has been noted (Zirschky and Wetherell 1987). Accidental exposures in the home have been reported in recent years in domestic industries (Meeks, Keith and Tanner 1990; Rowens et al. 1991) and in an accidental sill of metallic mercury (Florentine and Sanfilio 1991). Elemental mercury exposure occurs mainly by inhalation, while alkyl mercury can be absorbed by ingestion, inhalation or dermal contact.

In the best-studied episode of poisoning, sensory and motor dysfunction and mental retardation were found following very high exposures to methylmercury either in utero or from breast milk (Bakir et al. 1973). Maternal exposures resulted from ingestion of methylmercury that had been used as a fungicide on grain.

pesticides and Related Chemicals

Several hundred million tons of pesticides are produced worldwide each year. Herbicides, fungicides and insecticides are employed mainly in agriculture by developed countries to improve crop yield and quality. Wood preservatives are a much smaller, but still a major, art of the market. Home and garden use represents a relatively minor proportion of total consumption, but from the point of view of neonatal toxicity, domestic poisonings are perhaps the most numerous. Occupational exposure is also a potential source of indirect exposure to infants if a parent is involved in work that uses pesticides. Exposure to pesticides is possible through dermal absorption, inhalation and ingestion. More than 50 pesticides have been declared carcinogenic in animals (McConnell 1986).

Organochlorine pesticides include aromatic compounds, such as DDT (bis(4-chlorohenyl)-1,1,1-trichloroethane), and cyclodienes, such as dieldrin. DDT came into use in the early 1940s as an effective means to eliminate mosquitoes carrying malaria, an application that is still widely employed today in developing countries. Lindane is an organochlorine used widely to control body lice and in agriculture, especially in developing countries. olychlorinated bihenyls (CBs), another fat-soluble organochlorine mixture used since the 1940s, pose a potential health risk to young children exposed through breast milk and other contaminated foods. Both lindane and CBs are discussed separately in this chapter. olybrominated bihenyls (BBs) also have been detected in breast milk, almost exclusively in Michigan. Here, a fire-retardant inadvertently mixed into livestock feed in 1973-74 became widely dispersed across the state through dairy and meat products.

Chlordane has been used as a pesticide and as a termiticide in houses, where it is effective for decades, no doubt because of its persistence. Exposure to this chemical can be from dietary and direct respiratory or dermal absorption. Levels in human milk in Japan could be related both to diet and to how recently homes had been treated. Women living in homes treated more than two years earlier had chlordane levels in milk three times those of women living in untreated homes (Taguchi and Yakushiji 1988).

Diet is the main source of persistent organochlorines, but smoking, air and water may also contribute to exposure. This class of pesticides, also termed halogenated hydrocarbons, is quite persistent in the environment, since these are lipophilic, resistant to metabolism or biodegradation and exhibit low volatility. Several hundreds of m have been found in human and animal fat among those with highest exposures. Because of their reproductive toxicity in wildlife and their tendency to bioaccumulate, organochlorines have been largely banned or restricted in developed countries.

At very high doses, neurotoxicity has been observed with organochlorines, but potential long-term health effects are of more concern among humans. Although chronic health effects have not been widely documented, heatotoxicity, cancer and reproductive dysfunction have been found in experimental animals and in wildlife. Health concerns arise mainly from observations in animal studies of carcinogenesis and of profound changes in the liver and the immune system.

Organohoshates and carbamates are less persistent than the organochlorines and are the most widely used class of insecticides internationally. pesticides of this class are degraded relatively quickly in the environment and in the body. A number of the organohoshates and carbamates exhibit high acute neurotoxicity and in certain cases chronic neurotoxicity as well. Dermatitis is also a widely reported symptom of pesticide exposure.

The petroleum-based products used to apply some pesticides are also of potential concern. Chronic effects including haematooietic and other childhood cancers have been associated with parental or residential exposures to pesticides, but the epidemiological data are quite limited. Nevertheless, based on the data from animal studies, exposures to pesticides should be avoided.

For the newborn, a wide spectrum of exposure possibilities and toxic effects have been reported. Among children who required hospitalization for acute poisoning, most had inadvertently ingested pesticide products, while a significant number had been exposed while laying on sprayed carets (Casey, Thomson and Vale 1994; Zwiener and Ginsburg 1988). Contamination of workers’ clothing by pesticide dust or liquid has long been recognized. Therefore, this route provides ample opportunity for home exposures unless workers take proper hygienic precautions after work. For example, an entire family had elevated levels of chlordecone (Keone) in their blood, attributed to home laundering of a worker’s clothes (Grandjean and Bach 1986). Household exposure to TCDD (dioxin) has been documented by the occurrence of chloracne in the son and wife of two workers exposed in the aftermath of an explosion (Jensen, Sneddon and Walker 1972).

Most of the possible exposures to infants arise from pesticide applications within and around the home (Lewis, Fortmann and Camann 1994). Dust in home carets has been found to be extensively contaminated with numerous pesticides (Fenske et al. 1994). Much of reported home contamination has been attributed to flea extermination or to lawn and garden application of pesticides (Davis, Bronson and Garcia 1992). Infant absorption of chloryrifos after treatment of homes for fleas has been predicted to exceed safe levels. Indeed, indoor air levels following such fumigation procedures do not always rapidly diminish to safe levels.

Breast milk is a potential source of pesticide exposure for the neonate. Human milk contamination with pesticides, especially the organochlorines, has been known for decades. Occupational and environmental exposures can lead to significant pesticide contamination of breast milk (D’Ercole et al. 1976; McConnell 1986). Organochlorines, which in the past have been resent in breast milk at excessive levels, are declining in developed countries, paralleling the decline in adipose concentrations that has occurred after restriction of these compounds. Therefore, DDT contamination of human milk is now highest in developing countries. There is little evidence of organohoshates in breast milk. This may be attributable to properties of water solubility and raid metabolism of these compounds in the body.

Ingestion of water contaminated with pesticides is also a potential health risk for the neonate. This problem is most renounced where infant formula must be reared using water. Otherwise, commercial infant formulae are relatively free of contaminants (National Research Council 1993). Food contamination with pesticides may also lead to infant exposure. Contamination of commercial milk, fruits and vegetables with pesticides exists at very low levels even in developed countries where regulation and monitoring are most vigorous (The Referee 1994). Although milk comprises most of the infant diet, fruits (especially ales) and vegetables (especially carrots) are also consumed in a significant amount by young children and therefore represent a possible source of pesticide exposure.

In the industrialized countries, including the United States and western Europe, most of the organochlorine pesticides, including DDT, chlordane, dieldrin and lindane, have been either banned, suspended or restricted since the 1970s (Maxcy Rosenau-Last 1994). pesticides still used for agricultural and non-agricultural purposes are regulated in terms of their levels in foods, water and pharmaceutical products. As a result of this regulation, the levels of pesticides in adipose tissue and human milk have significantly declined over the past four decades. However, the organochlorines are still widely used in developing countries, where, for example, lindane and DDT are among the most frequently employed pesticides for agricultural use and for malaria control (Awumbila and Bokuma 1994).


Lindane is the γ-isomer and active ingredient of the technical grade of benzene hexachloride (BHC). BHC, also known as hexachlorocyclohexane (HCH), contains 40 to 90% of other isomers— α, β and δ. This organochlorine has been used as an agricultural and non-agricultural pesticide throughout the world since 1949. Occupational exposures may occur during the manufacture, formulation and application of BHC. Lindane as a pharmaceutical reparation in creams, lotions and shampoos is also widely used to treat scabies and body lice. Because these skin conditions commonly occur among infants and children, medical treatment can lead to absorption of BHC by infants through the skin. Neonatal exposure can also occur by inhalation of vapour or dust that may be brought home by a parent or that may linger after home use. Dietary intake is also a possible means of exposure to infants since BHC has been detected in human milk, dairy products and other foods, as have many organochlorine insecticides. Exposure through breast milk was more prevalent in the United States prior to the ban on the commercial production of lindane. According to the IARC (International Agency for Research on Cancer 1987), it is possible that hexachlorocyclohexane is carcinogenic to humans. However, evidence for adverse health outcomes among infants has been reported chiefly as effects on the neurological and haematooietic systems.

Household exposure to lindane has been described in the wife of a pesticide formulator, demonstrating the potential for similar neonatal exposures. The wife had 5 ng/ml of γ-BHC in her blood, a concentration lower than that of her husband (table 1) (Starr et al. 1974). presumably, γ-BHC was brought into the home on the body and/or clothes of the worker. Levels of γ-BHC in the woman and her husband were higher than those reported in children treated with lotion containing 0.3 to 1.0% BHC.

BHC in breast milk exists mainly as the β-isomer (Smith 1991). The half-life of the γ-isomer in the human body is approximately one day, while the β-isomer accumulates.

Table 1. Potential sources and levels of exposure to newborns

  Source of exposure g-BHC in blood
(ng/ml; ppb)
Occupational exposures Low exposures
High exposures
Adult male Attempted suicide 1300
Child Acute poisoning 100-800
Children 1% BHC lotion (average) 13
Case report of home exposure1 Husband
Unexposed populations since1980 Yugoslavia

1Starr et al. (1974); other data from Smith (1991).
2Largely b-isomer.

Dermal absorption of lindane from pharmaceutical products is a function of the amount applied to the skin and duration of exposure. Compared with adults, infants and young children appear to be more susceptible to the toxic effects of lindane (Clement International Corporation 1992). One reason may be that dermal absorption is enhanced by increased permeability of the infant’s skin and a large surface-to-volume ratio. Levels in the neonate may persist longer because the metabolism of BHC is less efficient in infants and young children. In addition, exposure in neonates may be increased by licking or mouthing treated areas (Kramer et al. 1990). A hot shower or bath before dermal application of medical products may facilitate dermal absorption, thereby exacerbating toxicity.

In a number of reported cases of accidental lindane poisoning, overt toxic effects have been described, some in young children. In one case, a two-month-old infant died after multiple exposures to 1% lindane lotion, including a full-body application following a hot bath (Davies et al. 1983).

Lindane production and use is restricted in most developed countries. Lindane is still used extensively in other countries for agricultural purposes, as noted in a study of pesticide use on farms in Ghana, where lindane accounted for 35 and 85% of pesticide use for farmers and herdsmen, respectively (Awumbila and Bokuma 1994).

olychlorinated bihenyls

olychlorinated bihenyls were used from the mid-1940s until the late 1970s as insulating fluids in electrical capacitors and transformers. Residues are still resent in the environment because of pollution, which is due largely to improper disposal or accidental sills. Some equipment still in use or stored remains a potential source of contamination. An incident has been reported in which children had detectable levels of CBs in their blood following exposure while laying with capacitors (Wolff and Schecter 1991). Exposure in the wife of an exposed worker has also been reported (Fishbein and Wolff 1987).

In two studies of environmental exposures, re- and postnatal exposure to CBs has been associated with small but significant effects in children. In one study, slightly impaired motor development was detected among children whose mothers had immediate postnatal breast milk CB levels in the upper 95th percentile of the study group (Rogan et al. 1986). In the other, sensory deficits (as well as smaller gestational size) were seen among children with blood levels in approximately the to 25% (Jacobson et al. 1985; Fein et al. 1984). These exposure levels were in the upper range for the studies (above 3 m in mother’s milk (fat basis) and above 3 ng/ml in children’s blood), yet these are not excessively high. Common occupational exposures result in levels ten to 100 times higher (Wolff 1985). In both studies, effects were attributed to prenatal exposure. Such results however sound a cautionary note for unduly exposing neonates to such chemicals both pre- and postnatally.


Solvents are a group of volatile or semi-volatile liquids that are used mainly to dissolve other substances. Exposure to solvents can occur in manufacturing processes, for example hexane exposure during distillation of petroleum products. For most persons, exposures to solvents will arise while these are being used on the job or in the home. Common industrial applications include dry cleaning, degreasing, painting and paint removal, and printing. Within the home, direct contact with solvents is possible during use of products such as metal cleaners, dry cleaning products, paint thinners or sprays.

The major routes of exposure for solvents in both adults and infants are through respiratory and dermal absorption. Ingestion of breast milk is one means of neonatal exposure to solvents derived from the parent’s work. Because of the brief half-life of most solvents, their duration in breast milk will be similarly short. However, following maternal exposure, some solvents will be resent in breast milk at least for a short time (at least one half-life). Solvents that have been detected in breast milk include tetrachloroethylene, carbon disulhide and halothane (an anaesthetic). A detailed review of potential infant exposure to tetrachloroethylene (TCE) has concluded that levels in breast milk can easily exceed recommended health risk guidelines (Schreiber 1993). Excess risk was highest for infants whose mothers might be exposed in the workplace (58 to 600 per million persons). For the highest non-occupational exposures, excess risks of 36 to 220 per 10 million persons were estimated; such exposures can exist in homes directly above dry-cleaners. It was further estimated that milk concentrations of TCE would return to “normal” (re-exposure) levels four to eight weeks after cessation of exposure.

Non-occupational exposures are possible for the infant in the home where solvents or solvent-based products are used. Indoor air has very low, but consistently detectable, levels of solvents like tetrachloroethylene. Water may also contain volatile organic compounds of the same type.

Mineral Dusts and Fibres: Asbestos, Fibreglass, Rock Wool, Zeolites, Talc

Mineral dust and fibre exposure in the workplace causes respiratory disease, including lung cancer, among workers. Dust exposure is a potential problem for the newborn if a parent carries articles into the home on the clothes or body. With asbestos, fibres from the workplace have been found in the home environment, and resulting exposures of family members have been termed bystander or family exposures. Documentation of familial asbestos disease has been possible because of the occurrence of a signal tumour, mesothelioma, that is primarily associated with asbestos exposure. Mesothelioma is a cancer of the leura or eritoneum (linings of lung and abdomen, respectively) that occurs following a long latency period, typically 30 to 40 years after the first asbestos exposure. The aetiology of this disease appears to be related only to the length of time after initial exposure, not to intensity or duration, nor to age at first exposure (Nicholson 1986; Otte, Sigsgaard and Kjaerulff 1990). Respiratory abnormalities have also been attributed to bystander asbestos exposure (Grandjean and Bach 1986). Extensive animal experiments support the human observations.

Most cases of familial mesothelioma have been reported among wives of exposed miners, millers, manufacturers and insulators. However, a number of childhood exposures have also been associated with disease. Quite a few of these children had initial contact that occurred at an early age (Dawson et al. 1992; Anderson et al. 1976; Roggli and Longo 1991). For example, in one investigation of 24 familial contacts with mesothelioma who lived in a crocidolite asbestos mining town, seven cases were identified whose ages were 29 to 39 years at diagnosis or death and whose initial exposure had occurred at less than one year of age (n=5) or at three years (n=2) (Hansen et al. 1993).

Exposure to asbestos is clearly causative for mesothelioma, but an epigenetic mechanism has been further pro[osed to account for unusual clustering of cases within certain families. Thus, the occurrence of mesothelioma among 64 persons in 27 families suggests a genetic trait that may render certain individuals more sensitive to the asbestos insult leading to this disease (Dawson et al. 1992; Bianchi, Brollo and Zuch 1993). However, it also has been suggested that exposure alone may provide an adequate explanation for the reported familial aggregation (Alderson 1986).

Other inorganic dusts associated with occupational disease include fibreglass, zeolites and talc. Both asbestos and fibreglass have been widely used as insulating materials. pulmonary fibrosis and cancer are associated with asbestos and much less clearly with fibreglass. Mesothelioma has been reported in areas of Turkey with indigenous exposures to natural zeolites. Exposures to asbestos may also arise from non-occupational sources. Diaers (“naies”) constructed from asbestos fibre were implicated as a source of childhood asbestos exposure (Li, Dreyfus and Antman 1989); however, parental clothing was not excluded as a source of asbestos contact in this report. Asbestos also has been found in cigarettes, hairdryers, floor tiles and some types of talcum powder. Its use has been eliminated in many countries. However, an important consideration for children is residual asbestos insulation in schools, which has been widely investigated as a potential public health problem.

Environmental Tobacco Smoke

Environmental tobacco smoke (ETS) is a combination of exhaled smoke and smoke emitted from the smoldering cigarette. Although ETS is not itself a source of occupational exposure that may affect the neonate, it is reviewed here because of its potential to cause adverse health effects and because it provides a good example of other aerosol exposures. Exposure of a non-smoker to ETS is often described as passive or involuntary smoking. prenatal exposure to ETS is clearly associated with deficits or impairments in foetal growth. It is difficult to distinguish postnatal outcomes from effects of ETS in the prenatal period, since parental smoking is rarely confined to one time or the other. However, there is evidence to support a relationship of postnatal exposure to ETS with respiratory illness and impaired lung function. The similarity of these findings to experiences among adults strengthens the association.

ETS has been well characterized and extensively studied in terms of human exposure and health effects. ETS is a human carcinogen (US Environmental protection Agency 1992). ETS exposure can be assessed by measuring levels of nicotine, a component of tobacco, and cotinine, its major metabolite, in biological fluids including saliva, blood and urine. Nicotine and cotinine have also been detected in breast milk. Cotinine has also been found in the blood and urine of infants who were exposed to ETS only by breast-feeding (Charlton 1994; National Research Council 1986).

Exposure of the neonate to ETS has been clearly established to result from paternal and maternal smoking in the home environment. Maternal smoking provides the most significant source. For example, in several studies urinary cotinine in children has been shown to correlate with the number of cigarettes smoked by the mother per day (Marbury, Hammon and Haley 1993). The major routes of ETS exposure for the neonate are respiratory and dietary (through breast milk). Day care centers represent another potential exposure situation; many child care facilities do not have a no-smoking policy (Sockrider and Coultras 1994).

Hospitalization for respiratory illness occurs more often among newborns whose parents smoke. In addition, the duration of hospital visits is longer among infants exposed to ETS. In terms of causation, ETS exposure has not been associated with specific respiratory diseases. There is evidence, however, that passive smoking increases the severity of re-existing illnesses such as bronchitis and asthma (Charlton 1994; Chilmonczyk et al. 1993; Rylander et al. 1993). Children and infants exposed to ETS also have higher frequencies of respiratory infections. In addition, smoking parents with respiratory illnesses can transmit airborne infections to infants by coughing.

Children exposed to ETS postnatally show small deficits in lung function which appear to be independent of prenatal exposures (Frischer et al. 1992). Although the ETS-related changes are small (0.5% decrement per year of forced expiratory volume), and while these effects are not clinically significant, they suggest changes in the cells of the developing lung that may portend later risk. parental smoking has also been associated with increased risk of otitis media, or middle ear effusion, in children from infancy to age nine. This condition is a common cause of deafness among children which can cause delays in educational progress. Associated risk is supported by studies attributing one-third of all cases of otitis media to parental smoking (Charlton 1994).

Radiation Exposures

Ionizing radiation exposure is an established health hazard which is generally the result of intense exposure, either accidental or for medical purposes. It can be damaging to highly proliferative cells, and can therefore be very harmful to the developing foetus or neonate. Radiation exposures that result from diagnostic x rays are generally very low level, and considered to be safe. A potential household source of exposure to ionizing radiation is radon, which exists in certain geographic areas in rock formations.

prenatal and postnatal effects of radiation include mental retardation, lower intelligence, growth retardation, congenital malformations and cancer. Exposure to high doses of ionizing radiation is also associated with increased prevalence of cancer. Incidence for this exposure is dependent upon dose and age. In fact, the highest relative risk observed for breast cancer (~9) is among women who were exposed to ionizing radiation at a young age.

Recently, attention has focused on the possible effects of non-ionizing radiation, or electromagnetic fields (EMF). The basis of a relationship between EMF exposure and cancer is not yet known, and the epidemiological evidence is still unclear. However, in several international studies an association has been reported between EMF and leukaemia and male breast cancer.

Childhood exposure to excessive sunlight has been associated with skin cancer and melanoma (Marks 1988).

Childhood Cancer

Although specific substances have not been identified, parental occupational exposures have been linked to childhood cancer. The latency period for developing childhood leukaemia can be two to 10 years following the onset of exposure, indicating that exposures in utero or in the early postnatal period may be implicated in the cause of this disease. Exposure to a number of organochlorine pesticides (BHC, DDT, chlordane) has been tentatively associated with leukaemia, although these data have not been confirmed in more detailed studies. Moreover, elevated risk of cancer and leukaemia has been reported for children whose parents engage in work that involves pesticides, chemicals and fumes (O’Leary et al. 1991). Similarly, risk of Ewing’s bone sarcoma in children was associated with parental occupations in agriculture or exposure to herbicides and pesticides (Holly et al. 1992).


Many nations attempt to regulate safe levels of toxic chemicals in ambient air and food products and in the workplace. Nevertheless, opportunities for exposure abound, and children are particularly susceptible to both absorption and to effects of toxic chemicals. It has been noted that “many of the 40,000 child lives lost in the developing world every day are a consequence of environmental abuses reflected in unsafe water supplies, disease, and malnutrition” (Schaefer 1994). Many environmental exposures are avoidable. Therefore, prevention of environmental diseases takes high priority as a defence against adverse health effects among children.



Read 3635 times Last modified on Tuesday, 11 October 2011 20:44


Part I. The Body
Cardiovascular System
Digestive System
Mental Health
Musculoskeletal System
Nervous System
Renal-Urinary System
Reproductive System
Respiratory System
Sensory Systems
Skin Diseases
Systematic Conditions
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Reproductive System Additional Resources

Click the Button below to view additional resources for this topic.


Reproductive System References

Agency for Toxic Substance and Disease Registry. 1992. Mercury toxicity. Am Fam Phys 46(6):1731-1741.

Ahlborg, JR, L Bodin, and C Hogstedt. 1990. Heavy lifting during pregnancy–A hazard to the fetus? A prospective study. Int J Epidemiol 19:90-97.

Alderson, M. 1986. Occupational Cancer. London: Butterworths.
Anderson, HA, R Lilis, SM Daum, AS Fischbein, and IJ Selikoff. 1976. Household contact asbestos neoplastic risk. Ann NY Acad Sci 271:311-332.

Apostoli, P, L Romeo, E Peroni, A Ferioli, S Ferrari, F Pasini, and F Aprili. 1989. Steroid hormone sulphation in lead workers. Br J Ind Med 46:204-208.

Assennato, G, C Paci, ME Baser, R Molinini, RG Candela, BM Altmura, and R Giogino. 1986. Sperm count suppression with endocrine dysfunction in lead-exposed men. Arch Environ Health 41:387-390.

Awumbila, B and E Bokuma. 1994. Survey of pesticides used in the control of ectoparasites on farm animals in Ghana. Tropic Animal Health Prod 26(1):7-12.

Baker, HWG, TJ Worgul, RJ Santen, LS Jefferson, and CW Bardin. 1977. Effect of prolactin on nuclear androgens in perifused male accessory sex organs. In The Testis in Normal and Infertile Men, edited by P and HN Troen. New York: Raven Press.

Bakir, F, SF Damluji, L Amin-Zaki, M Murtadha, A Khalidi, NY Al-Rawi, S Tikriti, HT Dhahir, TW Clarkson, JC Smith, and RA Doherty. 1973. Methyl mercury poisoning in Iraq. Science 181:230-241.

Bardin, CW. 1986. Pituitary-testicular axis. In Reproductive Endocrinology, edited by SSC Yen and RB Jaffe. Philadelphia: WB Saunders.

Bellinger, D, A Leviton, C Waternaux, H Needleman, and M Rabinowitz. 1987. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. New Engl J Med 316:1037-1043.

Bellinger, D, A Leviton, E Allred, and M Rabinowitz. 1994. Pre- and postnatal lead exposure and behavior problems in school-aged children. Environ Res 66:12-30.

Berkowitz, GS. 1981. An epidemiologic study of preterm delivery. Am J Epidemiol 113:81-92.

Bertucat, I, N Mamelle, and F Munoz. 1987. Conditions de travail des femmes enceintes–étude dans cinq secteurs d’activité de la région Rhône-Alpes. Arch mal prof méd trav secur soc 48:375-385.

Bianchi, C, A Brollo, and C Zuch. 1993. Asbestos-related familial mesothelioma. Eur J Cancer 2(3) (May):247-250.

Bonde, JPE. 1992. Subfertility in relation to welding–A case referent study among male welders. Danish Med Bull 37:105-108.

Bornschein, RL, J Grote, and T Mitchell. 1989. Effects of prenatal lead exposure on infant size at birth. In Lead Exposure and Child Development, edited by M Smith and L Grant. Boston: Kluwer Academic.

Brody, DJ, JL Pirkle, RA Kramer, KM Flegal, TD Matte, EW Gunter, and DC Pashal. 1994. Blood lead levels in the US population: Phase one of the Third National Health and Nutrition Examination survey (NHANES III, 1988 to 1991). J Am Med Assoc 272:277-283.

Casey, PB, JP Thompson, and JA Vale. 1994. Suspected paediatric poisoning in the UK; I-Home accident surveillance system 1982-1988. Hum Exp Toxicol 13:529-533.

Chapin, RE, SL Dutton, MD Ross, BM Sumrell, and JC Lamb IV. 1984. The effects of ethylene glycol monomethyl ether on testicular histology in F344 rats. J Androl 5:369-380.

Chapin, RE, SL Dutton, MD Ross, and JC Lamb IV. 1985. Effects of ethylene glycol monomethyl ether (EGME) on mating performance and epididymal sperm parameters in F344 rats. Fund Appl Toxicol 5:182-189.

Charlton, A. 1994. Children and passive smoking. J Fam Pract 38(3)(March):267-277.

Chia, SE, CN Ong, ST Lee, and FHM Tsakok. 1992. Blood concentrations of lead, cadmium, mercury, zinc, and copper and human semen parameters. Arch Androl 29(2):177-183.

Chisholm, JJ Jr. 1978. Fouling one’s nest. Pediatrics 62:614-617.

Chilmonczyk, BA, LM Salmun, KN Megathlin, LM Neveux, GE Palomaki, GJ Knight, AJ Pulkkinen, and JE Haddow. 1993. Association between exposure to environmental tobacco smoke and exacerbations of asthma in children. New Engl J Med 328:1665-1669.

Clarkson, TW, GF Nordberg, and PR Sager. 1985. Reproductive and developmental toxicity of metals. Scand J Work Environ Health 11:145-154.
Clement International Corporation. 1991. Toxicological Profile for Lead. Washington, DC: US Department of Health and Human Services, Public Health Service Agency for Toxic Substances and Disease Registry.

——. 1992. Toxicological Profile for A-, B-, G-, and D-Hexachlorocyclohexane. Washington, DC: US Department of Health and Human Services, Public Health Service Agency for Toxic Substances and Disease Registry.

Culler, MD and A Negro-Vilar. 1986. Evidence that pulsatile follicle-stimulating hormone secretion is independent of endogenous luteinizing hormone-releasing hormone. Endocrinology 118:609-612.

Dabeka, RW, KF Karpinski, AD McKenzie, and CD Bajdik. 1986. Survey of lead, cadmium and flouride in human milk and correlation of levels with environmental and food factors. Food Chem Toxicol 24:913-921.

Daniell, WE and TL Vaughn. 1988. Paternal employment in solvent related occupations and adverse pregnancy outcomes. Br J Ind Med 45:193-197.
Davies, JE, HV Dedhia, C Morgade, A Barquet, and HI Maibach. 1983. Lindane poisonings. Arch Dermatol 119 (Feb):142-144.

Davis, JR, RC Bronson, and R Garcia. 1992. Family pesticide use in the home, garden, orchard, and yard. Arch Environ Contam Toxicol 22(3):260-266.

Dawson, A, A Gibbs, K Browne, F Pooley, and M Griffiths. 1992. Familial mesothelioma. Details of seventeen cases with histopathologic findings and mineral analysis. Cancer 70(5):1183-1187.

D’Ercole, JA, RD Arthur, JD Cain, and BF Barrentine. 1976. Insecticide exposure of mothers and newborns in a rural agricultural area. Pediatrics 57(6):869-874.

Ehling, UH, L Machemer, W Buselmaier, J Dycka, H Froomberg, J Dratochvilova, R Lang, D Lorke, D Muller, J Peh, G Rohrborn, R Roll, M Schulze-Schencking, and H Wiemann. 1978. Standard protocol for the dominant lethal test on male mice. Arch Toxicol 39:173-185.

Evenson, DP. 1986. Flow cytometry of acridine orange stained sperm is a rapid and practical method for monitoring occupational exposure to genotoxicants. In Monitoring of Occupational Genotoxicants, edited by M Sorsa and H Norppa. New York: Alan R Liss.

Fabro, S. 1985. Drugs and male sexual function. Rep Toxicol Med Lettr 4:1-4.

Farfel, MR, JJ Chisholm Jr, and CA Rohde. 1994. The long-term effectiveness of residential lead paint abatement. Environ Res 66:217-221.

Fein, G, JL Jacobson, SL Jacobson, PM Schwartz, and JK Dowler. 1984. Prenatal exposure to polychlorinated biphenyls: effects on birth size and gestational age. J Pediat 105:315-320.

Fenske, RA, KG Black, KP Elkner, C Lee, MM Methner, and R Soto. 1994. Potential exposure and health risks of infants following indoor residential pesticide applications. Am J Public Health 80(6):689-693.

Fischbein, A and MS Wolff. 1987. Conjugal exposure to polychlorinated biphenyls (PCBs). Br J Ind Med 44:284-286.

Florentine, MJ and DJ II Sanfilippo. 1991. Elemental mercury poisoning. Clin Pharmacol 10(3):213-221.

Frischer, T, J Kuehr, R Meinert, W Karmaus, R Barth, E Hermann-Kunz, and R Urbanek. 1992. Maternal smoking in early childhood: A risk factor for bronchial responsiveness to exercise in primary-school children. J Pediat 121 (Jul):17-22.

Gardner, MJ, AJ Hall, and MP Snee. 1990. Methods and basic design of case-control study of leukemia and lymphoma among young people near Sellafield nuclear plant in West Cumbria. Br Med J 300:429-434.

Gold, EB and LE Sever. 1994. Childhood cancers associated with parental occupational exposures. Occup Med .

Goldman, LR and J Carra. 1994. Childhood lead poisoning in 1994. J Am Med Assoc 272(4):315-316.

Grandjean, P and E Bach. 1986. Indirect exposures: the significance of bystanders at work and at home. Am Ind Hyg Assoc J 47(12):819-824.
Hansen, J, NH de-Klerk, JL Eccles, AW Musk, and MS Hobbs. 1993. Malignant mesothelioma after environmental exposure to blue asbestos. Int J Cancer 54(4):578-581.

Hecht, NB. 1987. Detecting the effects of toxic agents on spermatogenesis using DNA probes. Environ Health Persp 74:31-40.
Holly, EA, DA Aston, DK Ahn, and JJ Kristiansen. 1992. Ewing’s bone sarcoma, paternal occupational exposure and other factors. Am J Epidemiol 135:122-129.

Homer, CJ, SA Beredford, and SA James. 1990. Work-related physical exertion and risk of preterm, low birthweight delivery. Paediat Perin Epidemiol 4:161-174.

International Agency for Research on Cancer (IARC). 1987. Monographs On the Evaluation of Carcinogenic Risks to Humans, Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs. Vol. 1-42, Suppl. 7. Lyon: IARC.

International Labour Organization (ILO). 1965. Maternity Protection: A World Survey of National Law and Practice. Extract from the Report of the Thirty-fifth Session of the Committee of Experts on the Application of Conventions and Recommendations, para. 199, note 1, p.235. Geneva:ILO.

——. 1988. Equality in Employment and Occupation, Report III (4B). International Labour Conference, 75th Session. Geneva: ILO.

Isenman, AW and LJ Warshaw. 1977. Guidelines On Pregnancy and Work. Chicago: American College of Obstetricians and Gynecologists.

Jacobson, SW, G Fein, JL Jacobson, PM Schwartz, and JK Dowler. 1985. The effect of intrauterine PCB exposure on visual recognition memory. Child Development 56:853-860.

Jensen, NE, IB Sneddon, and AE Walker. 1972. Tetrachlorobenzodioxin and chloracne. Trans St Johns Hosp Dermatol Soc 58:172-177.

Källén, B. 1988. Epidemiology of Human Reproduction. Boca Raton:CRC Press

Kaminski, M, C Rumeau, and D Schwartz. 1978. Alcohol consumption in pregnant women and the outcome of pregnancy. Alcohol, Clin Exp Res 2:155-163.

Kaye, WE, TE Novotny, and M Tucker. 1987. New ceramics-related industry implicated in elevated blood lead levels in children. Arch Environ Health 42:161-164.

Klebanoff, MA, PH Shiono, and JC Carey. 1990. The effect of physical activity during pregnancy on preterm delivery and birthweight. Am J Obstet Gynecol 163:1450-1456.

Kline, J, Z Stein, and M Susser. 1989. Conception to birth-epidemiology of prenatal development. Vol. 14. Monograph in Epidemiology and Biostatistics. New York: Oxford Univ. Press.

Kotsugi, F, SJ Winters, HS Keeping, B Attardi, H Oshima, and P Troen. 1988. Effects of inhibin from primate sertoli cells on follicle-stimulating hormone and luteinizing hormone release by perifused rat pituitary cells. Endocrinology 122:2796-2802.

Kramer, MS, TA Hutchinson, SA Rudnick, JM Leventhal, and AR Feinstein. 1990. Operational criteria for adverse drug reactions in evaluating suspected toxicity of a popular scabicide. Clin Pharmacol Ther 27(2):149-155.

Kristensen, P, LM Irgens, AK Daltveit, and A Andersen. 1993. Perinatal outcome among children of men exposed to lead and organic solvents in the printing industry. Am J Epidemiol 137:134-144.

Kucera, J. 1968. Exposure to fat solvents: A possible cause of sacral agenesis in man. J Pediat 72:857-859.

Landrigan, PJ and CC Campbell. 1991. Chemical and physical agents. Chap. 17 in Fetal and Neonatal Effects of Maternal Disease, edited by AY Sweet and EG Brown. St. Louis: Mosby Year Book.

Launer, LJ, J Villar, E Kestler, and M de Onis. 1990. The effect of maternal work on fetal growth and duration of pregnancy: a prospective study. Br J Obstet Gynaec 97:62-70.

Lewis, RG, RC Fortmann, and DE Camann. 1994. Evaluation of methods for monitoring the potential exposure of small children to pesticides in the residential environment. Arch Environ Contam Toxicol 26:37-46.

Li, FP, MG Dreyfus, and KH Antman. 1989. Asbestos-contaminated nappies and familial mesothelioma. Lancet 1:909-910.

Lindbohm, ML, K Hemminki, and P Kyyronen. 1984. Parental occupational exposure and spontaneous abortions in Finland. Am J Epidemiol 120:370-378.

Lindbohm, ML, K Hemminki, MG Bonhomme, A Anttila, K Rantala, P Heikkila, and MJ Rosenberg. 1991a. Effects of paternal occupational exposure on spontaneous abortions. Am J Public Health 81:1029-1033.

Lindbohm, ML, M Sallmen, A Antilla, H Taskinen, and K Hemminki. 1991b. Paternal occupational lead exposure and spontaneous abortion. Scand J Work Environ Health 17:95-103.

Luke, B, N Mamelle, L Keith, and F Munoz. 1995. The association between occupational factors and preterm birth in US nurses’ survey. Obstet Gynecol Ann 173(3):849-862.

Mamelle, N, I Bertucat, and F Munoz. 1989. Pregnant women at work: Rest periods to prevent preterm birth? Paediat Perin Epidemiol 3:19-28.

Mamelle, N, B Laumon, and PH Lazar. 1984. Prematurity and occupational activity during pregnancy. Am J Epidemiol 119:309-322.

Mamelle, N and F Munoz. 1987. Occupational working conditions and preterm birth: A reliable scoring system. Am J Epidemiol 126:150-152.

Mamelle, N, J Dreyfus, M Van Lierde, and R Renaud. 1982. Mode de vie et grossesse. J Gynecol Obstet Biol Reprod 11:55-63.

Mamelle, N, I Bertucat, JP Auray, and G Duru. 1986. Quelles mesures de la prevention de la prématurité en milieu professionel? Rev Epidemiol Santé Publ 34:286-293.

Marbury, MC, SK Hammon, and NJ Haley. 1993. Measuring exposure to environmental tobacco smoke in studies of acute health effects. Am J Epidemiol 137(10):1089-1097.

Marks, R. 1988. Role of childhood in the development of skin cancer. Aust Paediat J 24:337-338.

Martin, RH. 1983. A detailed method for obtaining preparations of human sperm chromosomes. Cytogenet Cell Genet 35:252-256.

Matsumoto, AM. 1989. Hormonal control of human spermatogenesis. In The Testis, edited by H Burger and D de Kretser. New York: Raven Press.

Mattison, DR, DR Plowchalk, MJ Meadows, AZ Al-Juburi, J Gandy, and A Malek. 1990. Reproductive toxicity: male and female reproductive systems as targets for chemical injury. Med Clin N Am 74:391-411.

Maxcy Rosenau-Last. 1994. Public Health and Preventive Medicine. New York: Appleton-Century-Crofts.

McConnell, R. 1986. Pesticides and related compounds. In Clinical Occupational Medicine, edited by L Rosenstock and MR Cullen. Philadelphia: WB Saunders.

McDonald, AD, JC McDonald, B Armstrong, NM Cherry, AD Nolin, and D Robert. 1988. Prematurity and work in pregnancy. Br J Ind Med 45:56-62.

——. 1989. Fathers’ occupation and pregnancy outcome. Br J Ind Med 46:329-333.

McLachlan, RL, AM Matsumoto, HG Burger, DM de Kretzer, and WJ Bremner. 1988. Relative roles of follicle-stimulating hormone and luteinizing hormone in the control of inhibin secretion in normal men. J Clin Invest 82:880-884.

Meeks, A, PR Keith, and MS Tanner. 1990. Nephrotic syndrome in two members of a family with mercury poisoning. J Trace Elements Electrol Health Dis 4(4):237-239.

National Reasearch Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: National Academy Press.

——. 1993. Pesticides in the Diets of Infants and Children. Washington, DC: National Academy Press.

Needleman, HL and D Bellinger. 1984. The developmental consequences of childhood exposure to lead. Adv Clin Child Psychol 7:195-220.

Nelson, K and LB Holmes. 1989. Malformations due to presumed spontaneous mutations in newborn infants. New Engl J Med 320(1):19-23.

Nicholson, WJ. 1986. Airborne Asbestos Health Assessment Update. Document No. EPS/600/8084/003F. Washington, DC: Environmental Criteria and Assessment.

O’Leary, LM, AM Hicks, JM Peters, and S London. 1991. Parental occupational exposures and risk of childhood cancer: a review. Am J Ind Med 20:17-35.

Olsen, J. 1983. Risk of exposure to teratogens amongst laboratory staff and painters. Danish Med Bull 30:24-28.

Olsen, JH, PDN Brown, G Schulgen, and OM Jensen. 1991. Parental employment at time of conception and risk of cancer in offspring. Eur J Cancer 27:958-965.

Otte, KE, TI Sigsgaard, and J Kjaerulff. 1990. Malignant mesothelioma clustering in a family producing asbestos cement in their home. Br J Ind Med 47:10-13.

Paul, M. 1993. Occupational and Environmental Reproductive Hazards: A Guide for Clinicians. Baltimore: Williams & Wilkins.

Peoples-Sheps, MD, E Siegel, CM Suchindran, H Origasa, A Ware, and A Barakat. 1991. Characteristics of maternal employment during pregnancy: Effects on low birthweight. Am J Public Health 81:1007-1012.

Pirkle, JL, DJ Brody, EW Gunter, RA Kramer, DC Paschal, KM Flegal, and TD Matte. 1994. The decline in blood lead levels in the United States. J Am Med Assoc 272 (Jul):284-291.

Plant, TM. 1988. Puberty in primates. In The Physiology of Reproduction, edited by E Knobil and JD Neill. New York: Raven Press.

Plowchalk, DR, MJ Meadows, and DR Mattison. 1992. Female reproductive toxicity. In Occupational and Environmental Reproductive Hazards: A Guide for Clinicians, edited by M Paul. Baltimore: Williams and Wilkins.

Potashnik, G and D Abeliovich. 1985. Chromosomal analysis and health status of children conceived to men during or following dibromochloropropane-induced spermatogenic suppression. Andrologia 17:291-296.

Rabinowitz, M, A Leviton, and H Needleman. 1985. Lead in milk and infant blood: A dose-response model. Arch Environ Health 40:283-286.

Ratcliffe, JM, SM Schrader, K Steenland, DE Clapp, T Turner, and RW Hornung. 1987. Semen quality in papaya workers with long term exposure to ethylene dibromide. Br J Ind Med 44:317-326.

Referee (The). 1994. J Assoc Anal Chem 18(8):1-16.

Rinehart, RD and Y Yanagisawa. 1993. Paraoccupational exposures to lead and tin carried by electric-cable splicers. Am Ind Hyg Assoc J 54(10):593-599.

Rodamilans, M, MJM Osaba, J To-Figueras, F Rivera Fillat, JM Marques, P Perez, and J Corbella. 1988. Lead toxicity on endocrine testicular function in an occupationally exposed population. Hum Toxicol 7:125-128.

Rogan, WJ, BC Gladen, JD McKinney, N Carreras, P Hardy, J Thullen, J Tingelstad, and M Tully. 1986. Neonatal effects of transplacental exposure to PCBs and DDE. J Pediat 109:335-341.

Roggli, VL and WE Longo. 1991. Mineral fiber content of lung tissue in patients with environmental exposures: household contacts vs. building occupants. Ann NY Acad Sci 643 (31 Dec):511-518.

Roper, WL. 1991. Preventing Lead Poisoning in Young Children: A Statement by the Centers for Disease Control. Washington, DC: US Department of Health and Human Services.

Rowens, B, D Guerrero-Betancourt, CA Gottlieb, RJ Boyes, and MS Eichenhorn. 1991. Respiratory failure and death following acute inhalation of mercury vapor. A clinical and histologic perspective. Chest 99(1):185-190.

Rylander, E, G Pershagen, M Eriksson, and L Nordvall. 1993. Parental smoking and other risk factors for wheezing bronchitis in children. Eur J Epidemiol 9(5):516-526.

Ryu, JE, EE Ziegler, and JS Fomon. 1978. Maternal lead exposure and blood lead concentration in infancy. J Pediat 93:476-478.

Ryu, JE, EE Ziegler, SE Nelson, and JS Fomon. 1983. Dietary intake of lead and blood lead concentration in early infancy. Am J Dis Child 137:886-891.

Sager, DB and DM Girard. 1994. Long term effects on reproductive parameters in female rats after translactional exposure to PCBs. Environ Res 66:52-76.

Sallmen, M, ML Lindbohm, A Anttila, H Taskinen, and K Hemminki. 1992. Paternal occupational lead exposure and congenital malformations. J Epidemiol Community Health 46(5):519-522.

Saurel-Cubizolles, MJ and M Kaminski. 1987. Pregnant women’s working conditions and their changes during pregnancy: A national study in France. Br J Ind Med 44:236-243.

Savitz, DA, NL Sonnerfeld, and AF Olshaw. 1994. Review of epidemiologic studies of paternal occupational exposure and spontaneous abortion. Am J Ind Med 25:361-383.

Savy-Moore, RJ and NB Schwartz. 1980. Differential control of FSH and LH secretion. Int Rev Physiol 22:203-248.

Schaefer, M. 1994. Children and toxic substances: Confronting a major public health challenge. Environ Health Persp 102 Suppl. 2:155-156.

Schenker, MB, SJ Samuels, RS Green, and P Wiggins. 1990. Adverse reproductive outcomes among female veterinarians. Am J Epidemiol 132 (January):96-106.

Schreiber, JS. 1993. Predicted infant exposure to tetrachloroethene in human breastmilk. Risk Anal 13(5):515-524.

Segal, S, H Yaffe, N Laufer, and M Ben-David. 1979. Male hyperprolactinemia: Effects on fertility. Fert Steril 32:556-561.

Selevan, SG. 1985. Design of pregnancy outcome studies of industrial exposures. In Occupational Hazards and Reproduction, edited by K Hemminki, M Sorsa, and H Vainio. Washington, DC: Hemisphere.

Sever, LE, ES Gilbert, NA Hessol, and JM McIntyre. 1988. A case-control study of congenital malformations and occupational exposure to low-level radiation. Am J Epidemiol 127:226-242.

Shannon, MW and JW Graef. 1992. Lead intoxication in infancy. Pediatrics 89:87-90.

Sharpe, RM. 1989. Follicle-stimulating hormone and spermatogenesis in the adult male. J Endocrinol 121:405-407.

Shepard, T, AG Fantel, and J Fitsimmons. 1989. Congenital defect abortuses: Twenty years of monitoring. Teratology 39:325-331.

Shilon, M, GF Paz, and ZT Homonnai. 1984. The use of phenoxybenzamine treatment in premature ejaculation. Fert Steril 42:659-661.

Smith, AG. 1991. Chlorinated hydrocarbon insecticides. In Handbook of Pesticide Toxicology, edited by WJ Hayes and ER Laws. New York: Acedemic Press.

Sockrider, MM and DB Coultras. 1994. Environmental tobacco smoke: a real and present danger. J Resp Dis 15(8):715-733.

Stachel, B, RC Dougherty, U Lahl, M Schlosser, and B Zeschmar. 1989. Toxic environmental chemicals in human semen: analytical method and case studies. Andrologia 21:282-291.

Starr, HG, FD Aldrich, WD McDougall III, and LM Mounce. 1974. Contribution of household dust to the human exposure to pesticides. Pest Monit J 8:209-212.

Stein, ZA, MW Susser, and G Saenger. 1975. Famine and Human Development. The Dutch Hunger Winter of 1944/45. New York: Oxford Univ. Press.

Taguchi, S and T Yakushiji. 1988. Influence of termite treatment in the home on the chlordane concentration in human milk. Arch Environ Contam Toxicol 17:65-71.

Taskinen, HK. 1993. Epidemiological studies in monitoring reproductive effects. Environ Health Persp 101 Suppl. 3:279-283.

Taskinen, H, A Antilla, ML Lindbohm, M Sallmen, and K Hemminki. 1989. Spontaneous abortions and congenital malformations among the wives of men occupationally exposed to organic solvents. Scand J Work Environ Health 15:345-352.

Teitelman, AM, LS Welch, KG Hellenbrand, and MB Bracken. 1990. The effects of maternal work activity on preterm birth and low birth weight. Am J Epidemiol 131:104-113.

Thorner, MO, CRW Edwards, JP Hanker, G Abraham, and GM Besser. 1977. Prolactin and gonadotropin interaction in the male. In The Testis in Normal and Infertile Men, edited by P Troen and H Nankin. New York :Raven Press.

US Environmental Protection Agency (US EPA). 1992. Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. Publication No. EPA/600/6-90/006F. Washington, DC: US EPA.

Veulemans, H, O Steeno, R Masschelein, and D Groesneken. 1993. Exposure to ethylene glycol ethers and spermatogenic disorders in man: A case-control study. Br J Ind Med 50:71-78.

Villar, J and JM Belizan. 1982. The relative contribution of prematurity and fetal growth retardation to low birth weight in developing and developed societies. Am J Obstet Gynecol 143(7):793-798.

Welch, LS, SM Schrader, TW Turner, and MR Cullen. 1988. Effects of exposure to ethylene glycol ethers on shipyard painters: ii. male reproduction. Am J Ind Med 14:509-526.

Whorton, D, TH Milby, RM Krauss, and HA Stubbs. 1979. Testicular function in DBCP exposed pesticide workers. J Occup Med 21:161-166.

Wilcox, AJ, CR Weinberg, JF O’Connor, DD BBaird, JP Schlatterer, RE Canfield, EG Armstrong, and BC Nisula. 1988. Incidence of early loss of pregnancy. New Engl J Med 319:189-194.

Wilkins, JR and T Sinks. 1990. Parental occupation and intracranial neoplasms of childhood: Results of a case-control interview study. Am J Epidemiol 132:275-292.

Wilson, JG. 1973. Environment and Birth Defects. New York: Academic Press.

——. 1977. current status of teratology-general principles and mechanisms derived from animal studies. In Handbook of Teratology, Volume 1, General Principles and Etiology, edited by JG Fraser and FC Wilson. New York: Plenum.

Winters, SJ. 1990. Inhibin is released together with testosterone by the human testis. J Clin Endocrinol Metabol 70:548-550.

Wolff, MS. 1985. Occupational exposure to polychlorinated biphenyls. Environ Health Persp 60:133-138.

——. 1993. Lactation. In Occupational and Environmental Reproductive Hazards: A Guide for Clinicians, edited by M Paul. Baltimore: Williams & Wilkins.

Wolff, MS and A Schecter. 1991. Accidental exposure of children to polychlorinated biphenyls. Arch Environ Contam Toxicol 20:449-453.

World Health Organization (WHO). 1969. Prevention of perinatal morbidity and mortality. Public Health Papers, No. 42. Geneva: WHO.

——. 1977. Modification Recommended by FIGO. WHO recommended definitions, terminology and format for statistical tables related to the perinatal period and use of a new certificate for cause of perinatal death. Acta Obstet Gynecol Scand 56:247-253.

Zaneveld, LJD. 1978. The biology of human spermatozoa. Obstet Gynecol Ann 7:15-40.

Ziegler, EE, BB Edwards, RL Jensen, KR Mahaffey, and JS Fomon. 1978. Absorption and retention of lead by infants. Pediat Res 12:29-34.

Zikarge, A. 1986. Cross-Sectional Study of Ethylene Dibromide-Induced Alterations of Seminal Plasma Biochemistry as a Function of Post-Testicular Toxicity with Relationships to Some Indices of Semen Analysis and Endocrine Profile. Dissertation, Houston, Texas: Univ.of Texas Health Science Center.

Zirschky, J and L Wetherell. 1987. Cleanup of mercury contamination of thermometer workers’ homes. Am Ind Hyg Assoc J 48:82-84.

Zukerman, Z, LJ Rodriguez-Rigau, DB Weiss, AK Chowdhury, KD Smith, and E Steinberger. 1978. Quantitative analysis of the seminiferous epithelium in human testicular biopsies, and the relation of spermatogenesis to sperm density. Fert Steril 30:448-455.

Zwiener, RJ and CM Ginsburg. 1988. Organophosphate and carbamate poisoning in infants and children. Pediatrics 81(1):121-126