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Preterm Delivery and Work

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The reconciliation of work and maternity is an important public health issue in industrialized countries, where more than 50% of women of child-bearing age work outside the home. Working women, unions, employers, politicians and clinicians are all searching for ways of preventing work-induced unfavourable reproductive outcomes. Women want to continue working while pregnant, and may even consider their physician’s advice about lifestyle modifications during pregnancy to be overprotective and unnecessarily restrictive.

physiological Consequences of pregnancy

At this point, it would be useful to review a few of the physiological consequences of pregnancy that may interfere with work.

A pregnant woman undergoes profound changes which allow her to adapt to the needs of the foetus. Most of these changes involve the modification of physiological functions that are sensitive to changes of posture or physical activity—the circulatory system, the respiratory system and water balance. As a result, physically active pregnant women may experience unique physiological and physiopathological reactions.

The main physiological, anatomical, and functional modifications undergone by pregnant women are (Mamelle et al. 1982):

  1. An increase in peripheral oxygen demand, leading to modification of the respiratory and circulatory systems. Tidal volume begins to increase in the third month and may amount to 40% of re-pregnancy values by the end of the pregnancy. The resultant increase in gas exchange may increase the hazard of the inhalation of toxic volatiles, while hyperventilation related to increased tidal volume may cause shortness of breath on exertion.
  2. Cardiac output increases from the very beginning of pregnancy, as a result of an increase in blood volume. This reduces the heart’s ability to adapt to exertion and also increases venous pressure in the lower limbs, rendering standing for long periods difficult.
  3. Anatomical modifications during pregnancy, including exaggeration of dorsolumbar lordosis, enlargement of the polygon of support and increases in abdominal volume, affect static activities.
  4. A variety of other functional modifications occur during pregnancy. Nausea and vomiting result in fatigue; daytime sleepiness results in inattention; mood changes and feelings of anxiety may lead to interpersonal conflicts.
  5. Finally, it is interesting to note that the daily energy requirements during pregnancy are equivalent to the requirements of two to four hours of work.

 

Because of these profound changes, occupational exposures may have special consequences in pregnant women and may result in unfavourable pregnancy outcomes.

Epidemiological Studies of Working Conditions and preterm Delivery

Although there are many possible unfavourable pregnancy outcomes, we review here the data on preterm delivery, defined as the birth of a child before the 37th week of gestation. preterm birth is associated with low birth weight and with significant complications for the newborn. It remains a major public health concern and is an ongoing reoccupation among obstetricians.

When we began research in this field in the mid-1980s, there was relatively strong legislative protection of pregnant women’s health in France, with prenatal maternity leave mandated to start six weeks prior to the due date. Although the preterm delivery rate has fallen from 10 to 7% since then, it appeared to have levelled off. Because medical prevention had apparently reached the limit of its powers, we investigated risk factors likely to be amenable to social intervention. Our hypotheses were as follows:

  • Is working per se a risk factor for preterm birth?
  • Are certain occupations associated with an increased risk of preterm delivery?
  • Do certain working conditions constitute a hazard to the pregnant woman and foetus?
  • Are there social preventive measures which could help reduce the risk of preterm birth?

 

Our first study, conducted in 1977–78 in two hospital maternity wards, examined 3,400 women, of whom 1,900 worked during pregnancy and 1,500 remained at home (Mamelle, Laumon and Lazar 1984). The women were interviewed immediately after delivery and asked to describe their home and work lifestyle during pregnancy as accurately as possible.

We obtained the following results:

Work per se

The mere fact of working outside the home cannot be considered to be a risk factor for preterm delivery, since women remaining at home exhibited a higher prematurely rate than did women who worked outside the home (7.2 versus 5.8%).

Working conditions

An excessively long work week appears to be a risk factor, since there was a regular increase in preterm delivery rate with the number of work hours. Retail-sector workers, medical social workers, specialized workers and service personnel were at higher risk of preterm delivery than were office workers, teachers, management, skilled workers or supervisors. The prematurely rates in the two groups were 8.3 and 3.8% respectively.

Table 1. Identified sources of occupational fatigue

Occupational fatigue index “HIGH” index if:
Posture Standing for more than 3 hours per day
Work on machines Work on industrial conveyor belts; independent work on industrial machines with strenuous effort
Physical load Continuous or periodical physical effort; carrying loads of more than 10kg
Mental load Routine work; varied tasks requiring little attention without stimulation
Environment Significant noise level; cold temperature; very wet atmosphere; handling of chemical substances

Source: Mamelle, Laumon and Lazar 1984.

Task analysis allowed identification of five sources of occupation fatigue: posture, work with industrial machines, physical workload, mental workload and the work environment. Each of these sources of occupational fatigue constitutes a risk factor for preterm delivery (see tables 1 and 2).

Table 2. Relative risks (RR) and fatigue indices for preterm delivery

Index Low index % High index % RR Statistical significance
Posture 4.5 7.2 1.6 Significant
Work on machines 5.6 8.8 1.6 Significant
Physical load 4.1 7.5 1.8 Highly significant
Mental load 4.0 7.8 2.0 Highly significant
Environment 4.9 9.4 1.9 Highly significant

Source: Mamelle, Laumon and Lazar 1984.

Exposure to multiple sources of fatigue may result in unfavourable pregnancy outcomes, as evidenced by the significant increase of the rate of preterm delivery with an increased number of sources of fatigue (table 3). Thus, 20% of women had concomitant exposure to at least three sources of fatigue, and experienced a preterm delivery rate twice as high as other women. Occupational fatigue and excessively long work weeks exert cumulative effects, such that women who experience intense fatigue during long work weeks exhibit an even higher prematurely rate. preterm delivery rates increase further if the woman also has a medical risk factor. The detection of occupational fatigue is therefore even more important than the detection of medical risk factors.

Table 3. Relative risk of prematurity according to number of occupational fatigue indices

Number of high
fatigue indices
Proportion of
exposed women %
Estimated
relative risk
0 24 1.0
1 28 2.2
2 25 2.4
3 15 4.1
4-5 8 4.8

Source: Mamelle, Laumon and Lazar 1984

European and North American studies have confirmed our results, and our fatigue scale has been shown to be reproducible in other surveys and countries.

In a case-control follow-u study conducted in France a few years later in the same maternity wards (Mamelle and Munoz 1987) , only two of the five previously defined indices of fatigue were significantly related to preterm delivery. It should however be noted that women had a greater opportunity to sit down and were withdrawn from physically demanding tasks as a result of preventive measures implemented in the workplaces during this period. The fatigue scale nevertheless remained a predictor of preterm delivery in this second study.

In a study in Montreal, Quebec (McDonald et al. 1988), 22,000 pregnant women were interviewed retrospectively about their working conditions. Long work weeks, alternating shift work and carrying heavy loads were all shown to exert significant effects. The other factors studied did not appear to be related to preterm delivery, although there appears to be a significant association between preterm delivery and a fatigue scale based on the total number of sources of fatigue.

With the exception of work with industrial machines, no significant association between working conditions and preterm delivery was found in a French retrospective study of a representative sample of 5,000 pregnant women (Saurel-Cubizolles and Kaminski 1987). However, a fatigue scale inspired by our own was found to be significantly associated with preterm delivery.

In the United States, Homer, Beredford and James (1990), in a historical cohort study, confirmed the association between physical workload and an increased risk of preterm delivery. Teitelman and co-workers (1990), in a prospective study of 1,200 pregnant women, whose work was classified as sedentary, active or standing, on the basis of job description, demonstrated an association between work in a standing position and preterm delivery.

Barbara Luke and co-workers (in press) conducted a retrospective study of US nurses who worked during pregnancy. Using our occupational risk scale, she obtained similar results to ours, that is, an association between preterm delivery and long work weeks, standing work, heavy workload and unfavourable work environment. In addition, the risk of preterm delivery was significantly higher among women with concomitant exposure to three or four sources of fatigue. It should be noted that this study included over half of all nurses in the United States.

Contradictory results have however been reported. These may be due to small sample sizes (Berkowitz 1981), different definitions of prematurely (Launer et al. 1990) and classification of working conditions on the basis of job description rather than actual workstation analysis (Klebanoff, Shiono and Carey 1990). In some cases, workstations have been characterized on a theoretical basis only—by the occupational physician, for example, rather than by the women themselves (peoples-Shes et al. 1991). We feel that it is important to take subjective fatigue—that is, fatigue as it is described and experienced by women—into account in the studies.

Finally, it is possible that the negative results are related to the implementation of preventive measures. This was the case in the prospective study of Ahlborg, Bodin and Hogstedt (1990), in which 3,900 active Swedish women completed a self-administered questionnaire at their first prenatal visit. The only reported risk factor for preterm delivery was carrying loads weighing more than 12 kg more often than 50 times per week, and even then the relative risk of 1.7 was not significant. Ahlborg himself points out that preventive measures in the form of aid maternity leave and the right to perform less tiring work during the two months receding their due date had been implemented for pregnant women engaged in tiring work. Maternity leaves were five times as frequent among women who described their work as tiring and involving the carrying of heavy loads. Ahlborg concludes that the risk of preterm delivery may have been minimized by these preventive measures.

preventive Interventions: French Examples

Are the results of aetiological studies convincing enough for preventive interventions to be applied and evaluated? The first question which must be answered is whether there is a public health justification for the application of social preventive measures designed to reduce the rate of preterm delivery.

Using data from our previous studies, we have estimated the proportion of preterm births caused by occupational factors. Assuming a rate of preterm delivery of 10% in populations exposed to intense fatigue and a rate of 4.5% in non-exposed populations, we estimate that 21% of premature births are caused by occupational factors. Reducing occupational fatigue could therefore result in the elimination of one-fifth of all preterm births in French working women. This is ample justification for the implementation of social preventive measures.

What preventive measures can be applied? The results of all the studies lead to the conclusion that working hours can be reduced, fatigue can be lessened through workstation modification, work breaks can be allowed and prenatal leave can be lengthened. Three cost-equivalent alternatives are available:

  • reducing the work week to 30 hours starting from the 20th week of gestation
  • prescribing a work break of one week each month starting in the 20th week of gestation
  • beginning prenatal leave at the 28th week of gestation.

 

It is relevant to recall here that French legislation provides the following preventive measures for pregnant women:

  • guaranteed employment after childbirth
  • reduction of the workday by 30 to 60 minutes, applied through collective agreements
  • workstation modification in cases of incompatibility with pregnancy
  • work breaks during pregnancy, prescribed by attending physicians
  • prenatal maternity leave six weeks prior to the due date, with a further two weeks available in case of complications
  • postnatal maternity leave of ten weeks.

 

A one-year prospective observational study of 23,000 women employed in 50 companies in the Rhône-Ales region of France (Bertucat, Mamelle and Munoz 1987) examined the effect of tiring work conditions on preterm delivery. Over the period of the study, 1,150 babies were born to the study population. We analysed the modifications of working conditions to accommodate pregnancy and the relation of these modifications to preterm delivery (Mamelle, Bertucat and Munoz 1989), and observed that:

  • Workstation modification was reformed for only 8% of women.
  • 33% of women worked their normal shifts, with the others having their workday reduced by 30 to 60 minutes.
  • 50% of women took at least one work break, apart from their prenatal maternity leave; fatigue was the cause in one-third of cases.
  • 90% of women stopped working before their legal maternity leave began and obtained at least the two weeks leave allowed for in the case of complications of pregnancy; fatigue was the cause in half the cases.
  • In all, given the legal prenatal leave period of six weeks prior to the due date (with an additional two weeks available in some cases), the real duration of prenatal maternity leave was 12 weeks in this population of women subjected to tiring work conditions.

 

Do these modifications of work have any effect on the outcome of pregnancy? Workstation modification and the slight reduction of the workday (30 to 60 min) were both associated with non-significant reductions of the risk of preterm delivery. We believe that further reductions of the work week would have a greater effect (table 4).

Table 4. Relative risks of prematurity associated with modifications in working conditions

Modifications
in working
conditions
Number of women Preterm
birth rates
(%)
Relative risk
(95% confidence intervals)
Change in work situation
No
Yes
1,062
87
6.2
3.4
0.5 (0.2-1.6)
Reduction of weekly working hours
No
Yes
388
761
7.7
5.1
0.7 (0.4-1.1)
Episodes of sick leave1
No
Yes
357
421
8.0
3.1
0.4 (0.2-0.7)
Increase of antenatal maternity leave1
None or only additional 2 weeks
Yes
487

291
4.3

7.2
1.7 (0.9-3.0)

1 In a reduced sample of 778 women with no previous or present obstetric pathology.

Source: Mamelle, Bertucat and Munoz 1989.

 

To analyse the relation between prenatal leave, work breaks and preterm delivery, it is necessary to discriminate between preventive and curative work breaks. This requires restriction of the analysis to women with uncomplicated pregnancies. Our analysis of this subgroup revealed a reduction of the preterm delivery rate among women who took work breaks during their pregnancy, but not in those who took prolonged prenatal leave (Table 9).

This observational study demonstrated that women who work in tiring conditions take more work breaks during their pregnancies than do other women, and that these breaks, particularly when motivated by intense fatigue, are associated with reductions of the risk of preterm delivery (Mamelle, Bertucat and Munoz 1989).

Choice of preventive Strategies in France

As epidemiologists, we would like to see these observations verified by experimental preventive studies. We must however ask ourselves which is more reasonable: to wait for such studies or to recommend social measures aimed at preventing preterm delivery now?

The French Government recently decided to include a “work and pregnancy guide”, identical to our fatigue scale, in each pregnant woman’s medical record. Women can thus calculate their fatigue score for themselves. If work conditions are arduous, they may ask the occupational physician or the person responsible for occupational safety in their company to implement modifications aimed at alleviating their workload. Should this be refused, they can ask their attending physician to prescribe rest weeks during their pregnancy, and even to prolong their prenatal maternity leave.

The challenge is now to identify preventive strategies that are well adapted to legislation and social conditions in every country. This requires a health economics approach to the evaluation and comparison of preventive strategies. Before any preventive measure can be considered generally applicable, many factors have to be taken into consideration. These include effectiveness, of course, but also low cost to the social security system, resultant job creation, women’s references and the acceptability to employers and unions.

This type of problem can be resolved using multicriteria methods such as the Electra method. These methods allow both the classification of preventive strategies on the basis of each of a series of criteria, and the weighting of the criteria on the basis of political considerations. Special importance can thus be given to low cost to the social security system or to the ability of women to choose, for example (Mamelle et al. 1986). While the strategies recommended by these methods vary depending on the decision makers and political options, effectiveness is always maintained from the public health standpoint.

 

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Contents

Preface
Part I. The Body
Blood
Cancer
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 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