Ethylbenzene-induced hearing loss, neurobehavioral function, and neurotransmitter alterations in petrochemical workers.

OBJECTIVE: To estimate hearing loss, neurobehavioral function, and neurotransmitter alteration induced by ethylbenzene in petrochemical workers. METHODS: From two petrochemical plants, 246 and 307 workers exposed to both ethylbenzene and noise were recruited-290 workers exposed to noise only from a power station plant and 327 office personnel as control group, respectively. Hearing and neurobehavioral functions were evaluated. Serum neurotransmitters were also determined. RESULTS: The prevalence of hearing loss was much higher in petrochemical groups than that in power station and control groups (P < 0.05). Compared with the control group, scores of neurobehavioral function reflecting learning and memory were decreased in petrochemical workers (P < 0.05), as well as acetylcholinesterase activity. Negative correlation was shown between neurobehavioral function and acetylcholinesterase. CONCLUSIONS: Ethylbenzene exposure might be associated with hearing loss, neurobehavioral function impairment, and imbalance of neurotransmitters.

[Role of laboratory tests in the early diagnosis of metabolic disorders in workers engaged in petrochemical production].

Studies of metabolic processes in petrochemical production workers revealed activation of lipid peroxidation, depressed antioxidant system, altered intracellular metabolism, high prevalence of dyslipidemia and increased serum enzymes levels. The metabolic changes of cellular and subcellular levels were seen in asymptomatic individuals--that supports value of laboratory tests in diagnosis of pathologic processes in petrochemical production workers.

[Contribution of polymorphic variants of the genes of xenobiotic transformation enzymes, antioxidative defense, and DNA repair to the development of individual predisposition to hepatobiliary and reproductive system diseases in petrochemical workers].

The paper gives the basic results of studying the polymorphic loci of the genes of xenobiotic transformation enzymes, antioxidative defense, and DNA repair in petrochemical workers. Polymerase chain reaction-restriction fragment length polymorphism assay was used to identify markers of the predisposition to the development of toxic hepatitis in men and impaired reproduction in women.

Nonalcoholic steatohepatitis: a toxic liver disease in industrial workers.

AIMS: Occupational/environmental exposure to hepatotoxins has recently been implicated in nonalcoholic steatohepatitis (NASH). The aims of this study were to determine the presence and frequency of NASH in a large group of workers chronically exposed to several volatile petrochemical products in an industrial area in north-east Brazil and to observe its course in workers removed from the work environment. METHODS: 1500 asymptomatic workers were screened with standard liver blood tests during 1994-5. Those with elevated transaminases (>3x normal) on 3 occasions were evaluated further both clinically and with serum HBsAg, anti-HCV, ferritin, lipids and autoantibody determination. Patients with either no etiological diagnosis, positive HBsAg/anti-HCV serology and/or excess alcohol intake underwent liver biopsy. Those with obesity, diabetes or an isolated abnormal GGT were excluded. Of workers diagnosed as having NASH (compatible histology and no excess alcohol intake), a proportion were removed from the work environment and evaluated monthly with liver blood tests and a repeat liver biopsy 8-14 months later. RESULTS: 112 workers had abnormal transaminases and 32 fulfilled the criteria for liver biopsy. 20 of these were classified as NASH, the remainder had viral hepatitis (n = 6), alcoholic liver disease (n = 5) or portal vein thrombosis (n = 1). In all of the 10/20 who were removed from the work environment, their aminotransferases and GGT gradually decreased and their histology improved. CONCLUSIONS: These results demonstrate that NASH can occur following chronic exposure to volatile petrochemical substances in the workplace. Exposed workers should be regularly screened for the presence of liver damage and ideally removed from the work environment where possible.

Lead intoxication among demolition workers: the effect of lead on the hepatic cytochrome P-450 system in humans.

Overt clinical disease from undue lead exposure has become a relatively rare phenomenon in adult populations. However, exposure situations that may result in subclinical disease are not uncommon in various occupational settings. Five demolition workers, dismantling an old iron structure covered with lead-content paint, were studied. The use of cutting torches resulted in lead fumes, with significant exposure, albeit without gross 'lead poisoning." All five workers showed biochemical manifestations of chronic lead intoxication-that is, elevated blood lead level, inhibition of delta-aminolevulinic acid dehydratase (ALA-D), and elevated erythrocytic protoporphyrin concentration (PROTO). The effect of lead on the biosynthesis of heme was assessed by investigating the functional capacity of the cytochrome P-45O system of the liver, through drug metabolism studies. The plasma elimination rates (half-lives) of antipyrine and phenylbutazone-drugs primarily metabolized by the hemeprotein P-450 dependent hepatic microsomal enzyme system-were measured before and after chelation therapy. Prior to chelation therapy all half-lives were within the normal range. A slight decrease in the half-life of antipyrine was found after treatment. These studies show that chronic exposure to lead has only a minimal effect on hepatic cytochrome p-450 dependent enzymatic activities in adult males.

Lead intoxication: effects on cytochrome P-450-mediated hepatic oxidations.

Acute administration of lead to rats caused significant decreases in cytochrome P=450, ethylmorphine N-demethylase, and aniline hydroxylase activities and prolonged hexobarbital-induced sleeping times. However, chronic administration of lead to weanling rats caused no significant changes in hepatic cytochrome P-450 levels or in the microsomal oxidative enzymes over a 12-wk period. Eight patients exposed to lead in the process of burning through lead-painted steel structures for at least 3 mo showed marked effects of chronic lead intoxication on the erythropoietic system: inhibition of erythrocyte delta-aminolevulinic acid dehydratase, increased erythrocyte protoporphyrin levels, and increased urinary excretion of delta-aminolevulinic acid. Chelation therapy greatly alleviated the inhibitory effects on dehydratase activity and decreased urinary delta-aminolevulinic acid excretion. The plasma elimination rate of antipyrine, a drug primarily metabolized by hepatic microsomal enzymes, was determined in the 8 subjects prior to and following chelation therapy. In 7 of 8 subjects, chelation therapy shortened the antipyrine half-lives, but the effect was minimal. These studies show that chronic lead exposure results in significant hematopoietic inhibition of the heme biosynthetic pathway without causing significant changes in hepatic cytochrome P-450-associated enzymic activities.