Reproductive toxicology in occupational settings: an update.
OBJECTIVE
This article mainly attempts to review the recent human literature on the adverse effects of occupational factors on fertility, developmental effects and genetic changes in the germ line, which lead to genetic malformations or to genetic disease. The secondary study aim is to answer whether occupational exposures are quantitative momentously for 15% involuntarily childless couples, 10-20% spontaneous abortions and 3% birth defects.


METHODS
A literature survey was conducted for publications on these subjects focusing on the latest publications. PubMed (Medline. 2005) was used for this literature search.


RESULTS
Publication bias and a large amount of confounding factors, which have to be controlled, make the design of human fertility studies difficult. Epidemiologic studies using time to conception techniques have been useful in identifying substances and exposure scenarios with proven toxic effect on fertility. The collected studies suggest that the exposure to the following substances or occupational settings may affect fertility function: lead, organic mercury compounds, manganese, carbon disulfide, 2-bromopropane and dibromochloropropane, welding, professional driving and working with heat. Concerning developmental effects even for methyl mercury, which was in group A of the German MAK list, to date no reliable evidence of the damaging effect on the human fetus under actual work conditions has been obtained. It is also difficult to classify substances according to their mutagenic potential for the germ cell, since no direct evidence of an association between exposure against a physical or chemical pollutant and the occurrence of a hereditary disorder has been found yet.


CONCLUSIONS
In conclusion there are only a few substances which may affect reproductive function in the workplace without a doubt. The decreasing fertility of women in Western countries can be explained by the increasing female reproduction age, rather than by occupational exposures. Also the rates for spontaneous abortions and birth defects cannot be explained by industrial exposures at the workplace.
Winker
R
R
Division of Occupational Medicine, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. robert.winker@meduniwien.ac.at
Rüdiger
H W
HW
D000022:Abortion, Spontaneous / Q000453:epidemiology; D000328:Adult; D000013:Congenital Abnormalities / Q000453:epidemiology; D005260:Female; D005298:Fertility / Q000235:genetics*; D005854:Germ Cells; D005858:Germany / Q000453:epidemiology; D006801:Humans; D008297:Male; D008452:Maximum Allowable Concentration; D008670:Metals / Q000506:poisoning; D009153:Mutagens; D016273:Occupational Exposure / Q000009:adverse effects*
D008670:Metals; D009153:Mutagens