In spite of the recognition of potentially toxic chemicals in chlorinated drinking water, few studies have evaluated reproductive health consequences of such exposure. Using data from a case-control study of miscarriage, preterm delivery, and low birth weight in central North Carolina, we evaluated risk associated with water source, amount, and trihalomethane (THM) concentration. Water source was not related to any of those pregnancy outcomes, but an increasing amount of ingested water was associated with decreased risks of all three outcomes (odds ratios around 1.5 for 0 glasses per day relative to 1-3 glasses per day, falling to 0.8 for 4+ glasses per day). THM concentration and dose (concentration x amount) were not related to pregnancy outcome, with the possible exception of an increased risk of miscarriage in the highest sextile of THM concentration (adjusted odds ratio = 2.8, 95% confidence interval = 1.1-2.7), which was not part of an overall dose-response gradient. These data do not indicate a strong association between chlorination by-products and adverse pregnancy outcome, but given the limited quality of our exposure assessment and the increased miscarriage risk in the highest exposure group, more refined evaluation is warranted.

Although the adverse effect on pregnancy outcomes at high levels of lead exposure in the workplace has been recognized for years, there is uncertainty regarding the impact of exposure at the lower community exposure levels commonly encountered today. This review summarizes the epidemiologic literature and discusses pertinent methodologic issues and possible sources of interstudy variation. The authors conclude that prenatal lead exposure is unlikely to increase the risk of premature membrane rupture but does appear to increase the risk of preterm delivery. Whether prenatal lead exposure decreases gestational age in terms of infants is unclear. Prenatal lead exposure also appears to be associated with reduced birth weight, but results vary in relation to study design and degree of control for confounding. Adjustment for gestational age, a possible confounder of the birth weight-lead exposure association, did not yield clearer results.

Exposure to benzene is generally accepted as a cause of acute myeloid leukemia (AML),

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Exposure to benzene is generally accepted as a cause of acute myeloid leukemia (AML), but the association with other cell types of leukemia and other lymphatic and hematopoietic cancers is controversial. We compiled epidemiologic research on benzene and lymphatic and hematopoietic cancers in order to assess the pattern of associations. Eighteen relevant community‐based and 16 industry‐based studies were located. Four of seven studies of lymphatic and hematopoietic cancer in the aggregate identified relative risks of 1.8 or more, and eight of 14 total leukemia studies yielded relative risks in that range. The few available studies of specific histologic types of leukemia do not indicate larger or more consistent elevations in risk for AML compared to other leukemia cell types. Sporadic reports have linked benzene to non‐Hodgkin's lymphoma and multiple myeloma, but most studies do not indicate a positive association. Limitations in study quality, particularly exposure assessment, pervade all of the studies reviewed, and the distinction between studies addressing benzene and those addressing jobs in industries that use benzene is somewhat arbitrary. Nonetheless, the epidemiologic evidence linking benzene to leukemia in the aggregate, as well as for subtypes other than AML, is no less persuasive than that for AML alone. Am. J. Ind. Med. 31:287–295, 1997. © 1997 Wiley‐Liss, Inc.