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Seroprevalence of human T lymphotropic virus (HTLV) and human immunodeficiency virus type 1 (HIV-1) was determined among 7841 intravenous drug users (IVDUs) from drug treatment centers in Baltimore, Chicago, Los Angeles, New Jersey (Asbury Park and Trenton), New York City (Brooklyn and Harlem), Philadelphia, and San Antonio, Texas; 20.9% had evidence of HTLV infection, as determined using a p21e EIA for screening and p21e blot for confirmation. With a type-specific EIA and blot used in combination, HTLV-II was identified in 97.6% of HTLV-positive IVDUs whose sera could be subtyped. HIV-1 seroprevalence was 13.2%. HTLV-II without HIV-1 was most common in Los Angeles and San Antonio. HIV-1 without HTLV-II was most common in New York, New Jersey, and Baltimore. Dual infection was most common in New York and New Jersey. Logistic regression analysis revealed that seroprevalence of HTLV-II was significantly greater with HIV-1 infection and increasing age and among women, blacks, and Mexican-Americans. In conclusion, it appears that among US IVDUs, nearly all HTLV infection is attributable to HTLV-II, and HTLV-II infection is associated with HIV-1 and sociodemographic background.

We pooled the data from 6 case-control studies of bladder cancer with detailed information on fluid intake and water pollutants, particularly trihalomethanes (THM), and evaluated the bladder cancer risk associated with total and specific fluid consumption. The analysis included 2,729 cases and 5,150 controls. Odds ratios (OR) and 95% confidence intervals (CI) for fluid consumption were adjusted for age, gender, study, smoking status, occupation and education. Total fluid intake was associated with an increased risk of bladder cancer in men. The adjusted OR for 1 l/day increase in intake was 1.08, (95% CI 1.03-1.14, p-value for linear trend0.001), while no trend was observed in women (OR=1.04, 0.94-1.15; p-value=0.7). OR was 1.33 (1.12-1.58) for men in the highest category of intake (3.5 l/day) as compared to those in the lowest (or=2 l/day). An increased risk was associated with intake of tap water. OR for2 l/day vs.or=0.5 l/day was 1.46 (1.20-1.78), with a higher risk among men (OR=1.50, 1.21-1.88). No increased risk was observed for the same intake groups of nontap water in men (OR=0.97, 0.77-1.22) or in women (OR=0.85, 0.50-1.42). Increased bladder cancer risks were observed for an intake of5 cups of coffee daily vs.5 and for THM exposure, but neither exposure confounded or modified the OR for tap water intake. The association of bladder cancer with tap water consumption, but not with nontap water fluids, suggests that carcinogenic chemicals in tap water may explain the increased risk.

Objective A recent study suggested that risk of bladder cancer may be higher in women than in men who smoked comparable amounts of cigarettes. We pooled primary data from 14 case-control studies of bladder cancer from Europe and North America and evaluated differences in risk of smoking by gender. Methods The pooled analysis included 8316 cases (21% women) and 17,406 controls (28% women) aged 30-79 years. Odds ratios (ORs) and 95% confidence intervals (95% CI) for smoking were adjusted for age and study. Exposure-response was evaluated in a stratified analysis by gender and by generalized additive models. Results The odds ratios for current smokers compared to nonsmokers were 3.9 (95% CI 3.5-4.3) for males and 3.6 (3.1-4.1) for females. In 11 out of 14 studies, ORs were slightly higher in men. ORs for current smoking were similar for men (OR = 3.4) and women (OR = 3.7) in North America, while in Europe men (OR = 5.3) had higher ORs than women (OR = 3.9). ORs increased with duration and intensity in both genders and the exposure-response patterns were remarkably similar between genders. Conclusion These results do not support the hypothesis that women have a higher relative risk of smoking-related bladder cancer than men.

Background Studies have suggested that risk of leukemia may be associated with occupational or industrial exposures and risk may vary by the histological type of the disease. Methods A population-based case-control study was conducted in Iowa and Minnesota to evaluate the association between various occupations, industries, and occupational exposures and leukemia risk. A total of 513 cases and 1,087 controls was included in the study. A lifetime occupational history and other risk factor information were collected through in-person interviews, and a job-exposure matrix was used to assess possible risks associated with specific exposures. Results A significantly increased risk of leukemia was observed among agricultural service industries and among nursing and healthcare workers. Janitors, cleaners, and light truck drivers also experienced increased risk. Those employed in plumbing, heating and air conditioning industries, and sales of nondurable goods (such as paints and varnishes) had an increased risk. Printers, painters, and workers in the food and metal industries had a nonsignificantly increased risk of leukemia. Analyses by specific exposures and histology of leukemia showed that risk of leukemia associated with occupational or industrial exposures may vary by histological type of the disease. Conclusions An increased risk of leukemia among workers employed in agricultural industries, nursing and healthcare workers, and in a few occupations with possible exposure to solvents is consistent with earlier studies. Associations of risk with occupations not observed previously deserve further assessment. Published 2001 Wiley-Liss, Inc.(dagger).

The etiology of non-Hodgkin’s lymphoma (NHL) is not well understood. To develop hypotheses on causes of this tumor, data from a population-based case-control interview study of 1,867 white men (622 cases and 1,245 controls) in Iowa and Minnesota conducted during 1980-1983 were examined. Subjects, or their next of kin, were interviewed to obtain information on agricultural exposures, work history, medical conditions, and family history. This analysis focuses on risks of NHL by occupation, by industry, and by selected exposures. Although many comparisons were made, few significant associations were observed. Small numbers and limitations in exposure assessment, however, would tend to reduce opportunities to detect associations. The strongest finding was with various occupations that work in metals and metal products. The analysis by exposure estimates also uncovered a significant association with metals, but risks did not increase with estimated intensity of exposure. Slightly elevated risks were also noted among persons employed as painters and construction workers, agricultural and forestry workers, printers and typesetters, funeral directors and embalmers, and dry cleaners. Although the overall risks for benzene and other solvents were small, they increased slightly with level of assigned exposure. Although some associations may be due to chance, several of these occupations and industries have been linked to lymphoma in other investigations and deserve further attention.

Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004–2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel9s full report (http://www.otru.org/pdf/special/expert_panel_tobacco_breast_cancer.pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex/current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N -acetyltransferase 2 gene ( NAT2 ) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality.

The risks of developing leukemia and non-Hodgkin’s lymphoma from living near industrial facilities were evaluated among men from Iowa and Minnesota in a population-based, case-control study. We found a statistically significant increase in the risk of developing non-Hodgkin’s lymphoma (RR = 1.4) and a slight, nonsignificant excess for leukemia (RR = 1.2) among individuals who lived .8-3.2 km (1/2-2 miles) from a factory. Risks were greater for certain histologic types: follicular lymphoma (RR = 1.5), acute lymphocytic leukemia (RR = 5.4), and acute myelocytic leukemia (RR = 2.2). For non-Hodgkin’s lymphoma (but not for leukemia), the relative risks for those living within .8 km (1/2 mile) of a factory were similar or slightly larger than for those living .8-3.2 km (1/2-2 miles) from a factory. Risks did not increase with duration of residence near a factory. The elevated risks of non-Hodgkin’s lymphoma were particularly associated with residing near stone, clay, or glass industry facilities. The risk of developing leukemia was greater among persons who resided near chemical and petroleum plants. These preliminary findings raise the possibility that general environmental exposure associated with certain industrial activities may elevate the risk of developing leukemia and non-Hodgkin’s lymphoma. Evaluation of data on proximity to industrial plants from studies in other geographic locations is needed to determine whether our results represent a meaningful association.