Trichlorethylene


Aluminum 
Ammonia 
Arsenic 
Cadmium 
Carbon Monoxide 
Chlordane 
Chlorpyrifos (Dursban) 
Chlorine 
Diesel Exhaust 
Epoxy Resins 
Formaldehyde 
Hydrogen Chloride 
Hydrogen Sulfide 
Nickel Carbonyl 
PCB's 
Pyrethrins 
Toluene 
Trichlorethylene 
Other Chemicals 

Background

 

 

Residents near two electronic manufacturing plants were frequently exposed to odorous chemicals for 4 to 40 years. Their high frequencies of many symptoms and excesses of cancer, birth defects and lupus erythematosus led to further investigation. Well-water and soil-gas contained trichloroethylene 1,1,1, trichloroethane, tetrachloroethylene and vinyl chloride. These chemicals have anesthetic properties and industrial exposures have caused coma suggesting that brain impairment might occur earlier than tumors or birth defects and should be the focus of study.

 

Methods

 

 

From the exposure zone (EZ) residents, 235 clients in a lawsuit and 58 non-clients were compared to 161 unexposed regional referents and to 69 residents outside this zone. These subjects affective status, symptoms frequencies, medical histories and exposure to chemicals at work and from the environment were also compared. Pulmonary functions were measured to assess possible contributions from air pollution.

 

Findings

 

 

Comparison of exposed subjects to referent showed significantly delayed simple and choice reaction times, impaired balance, delayed blink reflex latency R-1 (BRL R-1) and impaired color discrimination. Forced expiratory volume in one second was also reduced. EZ residents' cognitive function, perceptual motor speed and recall tested significantly worse than referents as did the scores on adverse moods. Frequencies of 31 of 35 neurobehavioral symptoms and respiratory and of rheumatic symptoms were elevated in exposed subjects. The differences were not attributed to bias or to confounding factors.

 

Conclusions

 

 

Contamination of residence area with chlorinated solvents for 40 years were associated with neurobehavioral impairment, pulmonary impairment and excessive symptom frequencies. As attempted remedial efforts, including soil and ground water stripping and other treatments since 1983 have neither reduced nor prevented residents' nervous system impairment, it may be necessary to relocate EZ subjects.

 

Group 2

 

 

Workers repairing jet engines had respiratory, rheumatic and neurobehavioral symptoms. They welded and ground stainless steel parts, using hard metal tools and cleaned metal with many solvents including chlorinated and fluorinated ones. We compared 154 workers and 112 referent subjects with similar ages and educational levels for reaction time, balance, blink reflex latency, color discrimination, Culture Fair, vocabulary, slotted pegboard, trail making A and B, profile of mood states (POMS), and did chest radiographs, spirometry and questionnaires. Workers compared to referents had significantly prolonged simple and choice reaction time (p<.0001), abnormal balance, with eyes open and eyes closed (p<.0001) and abnormal color discrimination. Blink reflex latency was abnormal in both exposed workers and in local referents compared to other reference groups. Respiratory and rheumatic symptom frequencies, POMS scores and depression were significantly greater in workers. Confounding factors were minimal and known biases were small. We tentatively attribute the neurobehavioral impairments and accompanying increased symptom frequencies to chlorinated solvent exposure. Excessive respiratory symptoms are attributed to welding stainless steel. Manganese exposure may have affected both respiratory and the central nervous system.

There are many reports of adverse effects of trichloroethylene on the cranial nerves particularly lengthening blink reflex latency. The mechanism responsible for global cerebral dysfunction in humans has not been elucidated but is consistent with astrocyte dysfunctions that adversely affect neurons to cause protracted and continuing ill effects. In two large population studies that of Phoenix, AZ, and of Tucson, AZ which preceding it, environmental residential exposures impaired blink, reaction time, balance, color vision, problem solving and memory functions. Thus, many of the brain functions were broadly diminished except that, well learned information, the domain most embedded, domain long-term memory, was intact. Mood state scores were elevated 2.5 times above unexposed people with depression and tension being most increased. The major conclusions of the study of the Phoenix neighbors of the Motorola plant where the TCE was dumped, were; (1) adverse effects were associated with nearness to the industrial releases of chemicals, (2) function tests of the plaintiffs in the lawsuit, their neighbors not in the lawsuit were not different. Plaintiffs were not biased towards abnormality. (3) the exposed individuals also had airways obstruction, (4) that the subjects who had lived in the area only after 1983, when Motorola claimed to have abated the problem, had intermediate degrees of impairment compared to those who had resided there for longer periods. This was consistent with their shorter durations of exposure, so that a reduction in doses of chemicals per year could not be inferred, (5) those subjects living in Northeast Phoenix outside the plume of exposure resembled unexposed referents except for having delayed blink reflex latency. This abnormality of a sentinel or marker for TCE and related chlorinated solvents suggests the peripheral spread of these chemicals.

 


Copyright (c) 2006 NTI. All rights reserved.