A case-control study of chronic neuropsychiatric disease and organic solvent exposure in automobile assembly plant workers.

Abstract

A case-control study of chronic neurological and psychiatric disease and occupational exposure to solvents was carried out in eight automobile assembly plants. Cases included 299 subjects who were granted medical disability retirement in 1980-8. Two control groups were selected, the first from those granted retirement in the same period because of medical disability from causes unrelated to solvent exposure. The second included hourly employees from the plant population. In these facilities, solvent exposures tended to be short term and low level, although common: the average duration of exposure was 2-3 years; about 41% experienced at least one day of exposure. Of those exposed, 46% had less than one year of exposure. Results for all psychiatric disease combined (273 cases) suggested that cases had lower exposures than either control group, regardless of how exposure was expressed. Results could not be explained by conventional confounding exposures or characteristics or by usual manifestations of the healthy worker effect. By contrast, chronic neurological disease, and multiple sclerosis in particular, seemed to be associated with exposure, although few cases -were identified and observed increases in risk were not statistically significant. (Occup Environ Med 1994;51:302-307)

Organic Solvents as Risk Factor for Autoimmune Diseases: A Systematic Review and Meta-Analysis

“…There were 5 studies showing complex data structure with different and non-cumulative results where the information for the different effects was not totally independent [52], [57], [70], [76], [78]. Then, 22 additional meta-analyses including 30 articles and the different outcomes of four of the above mentioned studies were calculated independently [57], [70], [76], [78].…”

“…Then, 22 additional meta-analyses including 30 articles and the different outcomes of four of the above mentioned studies were calculated independently [57], [70], [76], [78]. These analyses included five from Diot et al 2002 [76] (different toxic exposure measured: chlorinate, ketones, aromatic, toluene, TCE), one from Nelson et al 1994 [57] (control not disabled population) and Purdie et al 2011 [70] (a different cutoff point to disease criteria) and fifteen from Thompson et al 2002 [78] (different toxic exposure measured: toluene, benzene, white spirit, perchlorethylene, TCE, trichlorethane, vinyl chloride, urea formaldehyde, meta-phenylenediamene, bicromade, aromatic hydrocarbons, aliphatic hydrocarbons, fenfluramine, diethylpropion, L5 OH-tryptophan). In these meta-analyses, the studies that provided uniquely RR data were not included [52], [54] for statistical reasons.…”

Field survey on types of organic solvents used in enterprises of various sizes

“…Accordingly, health effects due to occupational solvent exposure are a focus of continuous attention. Whereas the health effects are typically on the central nervous system (Lee et al 1988;Liu et al 1988;Edling 1990;Cai et al 1991;Houck et al 1992;Uchida et al 1993;Ukai et al 1993;Nelson et al 1994;Ihrig et al 2005), effects on the liver (e.g., Fleming et al 1990), the kidneys (e.g., Franchini et al 1983;Ana-Lilia et al 2005;Voss et al 2005) and the peripheral nervous system (Inoue et al 1970;Cianchetti et al 1976;Takeuchi 1993) were also described, and even insidious effects on the reproductive functions (Huel et al 1990) as well as carcinogenicity (Chen and Seaton 1996) other than wellknown benzene-associated leukemia (Aksoy 1985) are suspected. One of the problems in the analysis for causative factors is variety of solvents used in workplaces.…”

Design, methodological issues and participation in a multiple sclerosis case-control study

“…While numerous putative environmental risk factors for MS have been studied, including infectious agents, toxic exposures and diet, findings are inconsistent . This inconsistency may be attributed to the difficulties of studying a complex disease with a heterogeneous clinical presentation and underlying pathology; long induction and latent periods between exposure and diagnosis; differences in relevant exposures from one population to another, possibly due to underlying genetic differences; and limitations of study design .…”