At present in India more than thirty mines are in operation. It produces 2800 tones of asbestos per month (mainly chrysotile and tremolite) and in recent years substantial quantity (-70%) is imported from Canada. The quality of asbestos produced in India is very poor. The mining and milling and other related processes expose the people to cancer and related diseases. Women are more affected by their exposure in processing unit compared to male who are generally working in mines. Direct and indirect employment in asbestos related industry and mine is around 100, 000 workers. Latency period (length of the time between exposure and the onset of diseases) in India is estimated to be 20-37 yr. The causes for lung and breathing problem are mainly due to obsolete technology and direct contact with the asbestos products without proper precaution, because in India asbestos are sold without statutory warning. This paper reviews health effects (such as fibrosis, sequelae, bronchogenic cancer, and malignant mesothelioma) on the Indian mine workers caused due to asbestos mining related activities with respect to their present day condition.
Platinosis with severe dermatitis and/or asthma is broadly defined as the effects of soluble platinum salts on people exposed to them occupationally. Platinum coordination complexes are widely used in the treatment of a variety of solid tumors. However, the clinical use of cisplatin, the most useful agent, is limited by the development of nephrotoxicity. Thus, an accidental exposure to soluble platinum at a high dose in platinum refineries and pharmaceutical factories could induce occupational nephrotoxicity. Urinary citrate is freely filtered at the glomerulus, and its reabsorption in the proximal tubule is the major determinant of the rate of renal excretion. In our previous studies, we found that the preincubation of rat renal brush border membrane vesicles (BBMV) with cisplatin and carboplatin, a second-generation platinum coordination complex, significantly inhibited the citrate uptake compared with that of the control BBMV. In this study, we performed in vivo expriments in cisplatin-intoxicated rats to elucidate the toxic mechanism of cisplatin. And our results showed that the citrate uptake was significantly inhibited in cisplatin-intoxicated rats at 1 min compared with that of control rats.
Recent studies suggest that moderate alcohol consumption is associated with a low risk of cancer, coronary heart disease, and other diseases. Most of these diseases are considered to be related to the action of reactive oxygen species (ROS) at certain stages of disease progression. However, considerable evidence exists indicating that ethanol generates ROS in vivo. Thus, the reduced risk of disease as a result of alcohol consumption seems to contradict evidence suggesting the induction of ROS by ethanol. In the present study, we investigated whether oxidative stress was induced in moderate alcohol drinkers. We measured the total urinary biopyrrins and 8-hydroxydeoxyguanosine (8-OHdG) levels as a systemic oxidative stress marker and an oxidative DNA damage marker, respectively. Serum uric acid was also measured as an alcohol-induced antioxidant. We compared total urinary biopyrrins and 8-OHdG levels among groups with different alcohol habits. The results showed that total biopyrrins levels increased with the amount of alcohol consumed, but that the level of 8-OHdG significantly decreased with the amount of alcohol consumed. The decrease in 8-OHdG levels seemed to be associated with increasing levels of uric acid. Judging from the increasing level of total biopyrrins, alcohol may induce ROS. ROS may then cause cell damage in liver, as suggested by the positive correlation between the total biopyrrins levels and the serum GOT, GPT, and γ-GTP levels. However, since ROS may be more effectively counteracted by uric acid in organs other than the liver, DNA damage may be surpressed rather than induced. Accordingly, moderate alcohol consumption seems to have the overall effect of reducing DNA damage, as shown by the decrease in urinary 8-OHdG levels observed in our study.
Exposure to benzene has been monitored in petrol-pump workers and dry cleaners of Meerut City (India) by measuring phenol content of their urine samples. Average values for phenol in urine were higher in petrol-pump workers than dry cleaners. Alcoholic subjects excreted more phenol than smokers and non-vegetarians. It is concluded that alcohol can alter the susceptibility of man to benzene toxicity by affecting its metabolism.
In order to investigate the cytokine profile in toluene diisocyanate (TDI)-induced occupational asthma, we conducted a quantification of cytokine production in a murine model of respiratory hyperreactivity to TDI. Wistar rats were sensitized with intranasal application of 10% TDI and provoked with 5% TDI to induce airway hypersensitivity. The blood leucocytes were counted, and bronchoalveolar lavage (BAL) was performed and the cellular responses in BAL fluid were analysed. Lung histological examination was performed to investigate the inflammatory status in the airway. The production of IL-2, IL-4, IL-6 and IFN-γ in serum, BAL fluid and spleen cell were determined with ELISA kits. The cellular results demonstrated that neutrophils and eosinophils in blood were significantly increased and the total cells and each different cell, in particular eosinophils in BAL fluid were markedly increased in TDI sensitized rats. Histological analysis showed that a respiratory inflammation represented by prominent infiltration of eosinophils in central and peripheral airways was present in TDI-sensitized rats. The cytokine assays revealed that in TDIsensitized rats, IL-4 was predominately secreted in serum, and IL-4 and IL-6 rather than IL-2 and IFN-γ were predominately secreted in BAL fluid and in spleen cell. These findings suggested that IL-4 and IL-6 are preferentially produced and may have an important role in occupational asthma induced by TDI.
A database of mutagenicity test results of new chemicals has been developed. Based on the amendment of the Industrial Safety and Health Law (ISHL) in 1979, manufacturers and importers in Japan are required to register any new work place chemicals with bacterial mutagenicity test results. At present more than ten thousand substances have been examined. We have surveyed correlations between 44 substructures and mutagenicity in 2, 857 ISHL data as well as in 1, 207 National Toxicology Program data as a preliminary analysis. The percentages of the mutagenic compounds were calculated. High percentages were found for electrophilic reagents such as epoxides(63%), aromatic nitro compounds(49%) and primary alkyl monohalides(46%). 71% of peroxides was found to be mutagenic. The results suggest that several types of reactions such as nucleophilic substitution reaction, nitrenium cation reaction and radical reaction are included in the process of the mutagenic alterations of DNA.
Acid anhydrides are low-molecular weight chemicals known to cause respiratory irritancy and allergy. Skin allergy has on rare occasions been reported. A total of 3 subjects with occupational exposure to methylhexahydrophthalic anhydride (MHHPA) and hexahydrophthalic anhydride (HHPA) from an epoxy resin system were studied to evaluate the nature of their reported skin and nose complaints (work-related anamnesis, specific IgE, contact urticaria examinations, and ambient monitoring). Using a Pharmacia CAP system with a HHPA human serum albumin conjugate, specific IgE antibody was detected in serum from 1 (33.3%) out of the 3 workers. One unsensitized worker displayed nasal pain and rhinorrhea only when loading liquid epoxy resins into the pouring-machine (2.2 mg MHHPA/m3 and 1.2 mg HHPA/m3), probably being an irritant reaction. Two workers had work-related symptoms at relatively low levels of exposure (geometric mean 32-103 μg MHHPA/m3 and 18-59 μg HHPA/m3); one complained of only rhinitis, and the other was sensitized against HHPA and displayed both rhinitis and contact urticaria (the face and neck). The worker's skin symptoms were evidently due to airborne contact, since she had not had any skin contact with liquid epoxy resin or mixtures of MHHPA and HHPA. These urticaria symptoms were confirmed by a 20-min closed patch test for MHHPA, but not by that for HHPA. The causative agent was considered to be MHHPA, although the specific IgE determination to MHHPA was not performed.
We encountered three patients (Patient I: 39-year-old man, Patient II: 34-year-old woman, and Patient III: 5-year-old girl) with acute methyl bromide poisoning, which had occurred as a result of exposure to the gas that leaked from methyl bromide cans stored in a warehouse of a seedling farm. Since all three patients exhibited almost the same initial symptoms, i.e., severe vomiting, tonic convulsions and clouding of consciousness, botulism was suspected at first. However, subsequent inquiry revealed that 27 cans of methyl bromide had been stored in the building that the patients lived in, and that the cans had been damaged a few days before the onset of the patients' illness by a thrashing machine that was being moved by them to another location. Inspection revealed that all the cans of methyl bromide had passed the expiry date and were corroded. Even though none of the cans had been used, three cans with a capacity of 750 g were found to be empty. Plasma bromide ion concentrations were determined to be high (72.9 μg/ml, 67.8 μg/ml and 91.5 μg/ml; normal level, <5 μg/ml), and acute methyl bromide poisoning was diagnosed 8 days after admission of the patients to the hospital. Hemodialysis (peritoneal lavage in the case of the child) was performed immediately, after which the plasma bromide ion concentrations returned to normal and the general condition of the patients gradually improved.