Neurotoxicity has been described in workers exposed to solvents, PCBs, certain metals, and polyaromatic hydrocarbons but not often in residents near refineries or factories. We compared the neurobehavioral performance of residents near a plant that reprocessed used motor oil and chemical waste from 1966-1983 to referents from beyond the plant's modeled air dispersal and water drainage zones. Neurophysiological and psychological tests, a Profile of Mood States (POMS) and a symptom questionnaire were administered to 131 subjects exposed at the site who were matched for age, sex, and ethnicity 2:1 with 66 unexposed subjects from 35 km away. Test scores were adjusted for a 1.4-year difference in educational attainment by coefficients from regression equations but not for income as the latter coefficients were not significant. Exposed subjects were significantly impaired for body balance (sway speed) and simple and two choice visual reaction time as compared to referents. Blink reflex latency (R-1) and eye closure speed were normal in both groups. Cognitive function in the exposed was impaired as measured by Culture Fair and by block design from the WAIS. Placing pegs in a grooved board and making of trails (A and B) were also impaired. Group differences in recall and memory were not significant. The exposed group's symptom frequencies and POMS scores for depression, anger, confusion, tension, and fatigue were elevated indicating depression. Confounding from medical and neurological disorders or occupational exposures was minimal. Subjects exposed residentially for up to 17 years to chemicals dispersed from a waste oil reprocessing plant showed neurophysiological and neuropsychological impairment.

Adolescent↗

PubMedDate not supplied

Effects of diesel exhaust on neurobehavioral and pulmonary functions.

Ten railroad workers and 6 electricians referred for shortness of breath also had slowness of response, memory loss, and disordered sleep, all of which suggested neurobehavioral impairment. The hypothesis was that diesel exhaust causes central nervous system impairment. Six electricians worked within enclosed concrete walls and roofs that trapped diesel exhaust from trucks. Seven railroad mechanics had tuned diesel engines indoors for 15-50 y, and 3 crewmen rode in locomotives. Neurobehavioral and visual functions were measured with a 26-test battery. Compared with unexposed men, the 16 in this study had significantly impaired reaction time, balance, blink reflex latency R-1, Culture Fair, peg placement, trail making, and verbal recall. Thirteen men had abnormal visual fields, and 11 had abnormal color confusion indices. Nine men had airways obstruction. The author could not attribute abnormalities to confounding factors or bias. Severe neurobehavioral impairment was associated with exposure to confined diesel exhaust. In additional studies of diesel-exposed workers, especially drivers of locomotives and trucks, investigators should use sensitive neurobehavioral methods.

Adult↗

PubMedDate not supplied

Chlorine-induced damage documented by neurophysiological, neuropsychological, and pulmonary testing.

Chlorine causes acute pulmonary edema and damages airways, thus producing obliterative bronchiolitis. In the case series in this study, its adverse effects were extended to visual and central nervous system impairment. Twenty-two patients exposed briefly to undiluted chlorine at home or work were evaluated with a battery of neurobehavioral and visual tests. Their test scores, expressed as percentage predicted, were compared with those of unexposed subjects. Chlorine-exposed subjects had impaired balance (with eyes open and eyes closed), delayed simple and choice reaction times, impaired color discrimination, impaired visual field performance, decreased hearing, and decreased grip strength. Blink reflex latency was delayed on the right. Cognitive performance (i.e., digit symbol and vocabulary), peg placement, trail making A and B, and verbal recall were significantly below predicted levels. Well-learned memory functions were not impaired. Adverse mood states scores were elevated as were the frequencies of 28 of 35 common symptoms. Forced vital capacities were reduced. The duration of chlorine exposures was from a breath or two to several hours, and exposures were associated with impaired neurophysiologic and neuropsychologic functions. Impairments appeared insidiously, were noted 1 to 48 mo after exposure, and persisted. Such functional losses must be prevented. Additional chlorine-exposed patients should be evaluated for neurological and pulmonary damage.

Adult↗

PubMedDate not supplied

Prevalence and features of advanced asbestosis (ILO profusion scores above 2/2). International Labour Office.

In this study, the author addressed the following question: Do workers with advanced asbestosis have a restrictive pulmonary physiology, and, alternately, do those who have restrictive physiological tests have advanced asbestosis? One group was identified by obvious radiographic measurements, and the other group was defined via physiologic measurements. Total lung capacity, vital capacity, and flows were measured in 12,856 men exposed to asbestos, of whom 3,445 had radiographic signs of asbestosis, as defined by the International Labour Office criteria. Radiographically advanced asbestosis-International Labour Office criteria profusion greater than 2/2 was present in 85 (2.5%) of men. An additional 52 men had physiologically restrictive disease. The author, who compared pulmonary flows and volumes of these two groups, used mean percentage predicted, adjusted for height, age, and duration of cigarette smoking. Men with radiographically advanced asbestosis had normal total lung capacity (i.e., 105.5% predicted), reduced forced vital capacities (i.e., 82.7% predicted), air trapping (i.e., residual volume/total lung capacity increased to 54.4%), and reduced flows (i.e., forced expiratory flow [FEF25-75] = 60.6% predicted, forced expiratory volume in 1 s = 78.0% predicted, and forced expiratory volume in 1 s/forced vital capacity = 65.5%). In contrast, men selected from the same exposed population for restrictive disease (i.e., reduced total lung capacity [72.6% predicted] and forced vital capacity [61.5% predicted]) also had airflow obstruction (i.e., forced expiratory volume in 1 s/forced vital capacity of 74.5% predicted) and air trapping (i.e., residual volume/total lung capacity of 46.7%). Only half of these men had asbestosis--and it was of minimal severity. In summary, advanced asbestosis was characterized by airway obstruction and air trapping, both of which reduced vital capacity but not total lung capacity; therefore, it was not a restrictive disease. In contrast, restrictive disease was rare and was associated with minimal asbestosis.

Aged↗

PubMedDate not supplied

A paradigm for environmental epidemiology: why are effects of environmental exposures different from occupational effects?

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California↗

PubMedDate not supplied

Function testing for chemical brain damage: a review.

Testing of neurobehavioral functions for evaluation of the effects of chemicals on the human brain from community (i.e., environmental) exposures is logical and may be a preferred initial step. Sensitivity is improved (1) by adjusting individual tests for influential factors, found by regression modeling and by retaining significant coefficients; and (2) by the calculation of predicted values for each test for each subject. This two-part approach allows for adjustments in age, sex, educational level, and other factors before comparisons are made. Visual fields, color discrimination, reaction time, balance, and digit symbol are the most sensitive tests, followed by 6 sensitive psychological tests and less-discriminating physiological measurements. Hydrogen sulfide, polychlorinated biphenyls, and arsenic are the most toxic chemicals, followed by chlorine, chlorpyrifos, formaldehyde, nickel carbonyl, and ammonia. The least toxic chemicals, which are hydrochloric acid and chlorine, were determined 7 wk following a community spill. The least toxic chemical among those identified herein is methyl ter butyl ether.

Brain Damage, Chronic↗

PubMedDate not supplied

Embryo toxicity and teratogenicity of formaldehyde.

C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as a methyl group into nucleic acids and proteins. Also, formaldehyde reacts chemically with organic compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein crosslinks. The following questions must be addressed: What adducts (e.g., N-methyl amino acids) are formed in the blood following formaldehyde inhalation? What role do N-methyl-amino adducts play in alkylation of nuclear and mitochondrial deoxyribonucleic acid, as well as mitochondrial peroxidation? The fact that the free formaldehyde pool in blood is not affected following exposure to the chemical does not mean that formaldehyde is not involved in altering cell and deoxyribonucleic acid characteristics beyond the nasal cavity. The teratogenic effect of formaldehyde in the English literature has been sought, beginning on the 6th day of pregnancy (i.e., rodents) (Saillenfait AM, et al. Food Chem Toxicol 1989, pp 545-48; Martin WJ. Reprod Toxicol 1990, pp 237-39; Ulsamer AG, et al. Hazard Assessment of Chemicals; Academic Press, 1984, pp 337-400; and U.S. Department of Health and Human Services. Toxicological Profile of Formaldehyde; ATSDR, 1999 [references 1-4, respectively, herein]). The exposure regimen is critical and may account for the differences in outcomes. Pregnant rats were exposed (a) prior to mating, (b) during mating, (c) or during the entire gestation period. These regimens (a) increased embryo mortality; (b) increased fetal anomalies (i.e., cryptochordism and aberrant ossification centers); (c) decreased concentrations of ascorbic acid; and (d) caused abnormalities in enzymes of mitochondria, lysosomes, and the endoplasmic reticulum. The alterations in enzymatic activity persisted 4 mo following birth. In addition, formaldehyde caused metabolic acidosis, which was augmented by iron deficiency. Furthermore, newborns exposed to formaldehyde in utero had abnormal performances in open-field tests. Disparities in teratogenic effects of toxic chemicals are not unusual. For example, chlorpyrifos has not produced teratogenic effects in rats when mothers are exposed on days 6-15 (Katakura Y, et al. Br J Ind Med 1993, pp 176-82 [reference 5 herein]) of gestation (Breslin WJ, et al. Fund Appl Toxicol 1996, pp 119-30; and Hanley TR, et al. Toxicol Sci 2000, pp 100-08 [references 6 and 7, respectively, herein]). However, either changing the endpoints for measurement or exposing neonates during periods of neurogenesis (days 1-14 following birth) and during subsequent developmental periods produced adverse effects. These effects included neuroapoptosis, decreased deoxyribonucleic acid and ribonucleic acid synthesis, abnormalities in adenylyl cyclase cascade, and neurobehavioral effects (Johnson DE, et al. Brain Res Bull 1998, pp 143-47; Lassiter TL, et al. Toxicol Sci 1999, pp 92-100; Chakraborti TK, et al. Pharmacol Biochem Behav 1993, pp 219-24; Whitney KD, et al. Toxicol Appl Pharm 1995, pp 53-62; Chanda SM, et al. Pharmacol Biochem Behav 1996, pp 771-76; Dam K, et al. Devel Brain Res 1998, pp 39-45; Campbell CG, et al. Brain Res Bull 1997, pp 179-89; and Xong X, et al. Toxicol Appl Pharm 1997, pp 158-74 [references 8-15, respectively, herein]). Furthermore, the terata caused by thalidomide is a graphic human example in which the animal model and timing of exposure were key factors (Parman T, et al. Natl Med 1999, pp 582-85; and Brenner CA, et al. Mol Human Repro 1998, pp 887-92 [references 16 and 17, respectively, herein]). Thus, it appears that more sensitive endpoints (e.g., enzyme activity, generation of reactive oxygen species, timing of exposure) for the measurement of toxic effects of environmental agents on embryos, fetuses, and neonates are more coherent than are gross terata observations. The perinatal period from the end of organogenesis to the end of the neonatal period in humans approximates the 28th day of gestation to 4 wk postpartum. Therefore, researchers must investigate similar stages of development (e.g., neurogenesis occurs in the 3rd trimester in humans and neonatal days occur during days 1-14 in rats and mice, whereas guinea pigs behave more like humans). Finally, screening for teratogenic events should also include exposure of females before mating or shortly following mating. Such a regimen is fruitful inasmuch as environmental agents cause adverse effec

Animals↗

PubMedDate not supplied

Byssinosis, emphysema, and mortality of American textile workers.

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Aged↗

PubMedDate not supplied

Chronic disease in the workplace and the environment. Lung disease: lessons from the past--keys to the future.

A rich experience has provided specific and sensitive methods for identifying adverse effects of environmental agents. Many classic lessons have come from occupational health. We must now decide how to apply these to the unsolved problems of the prevalent chronic pulmonary diseases: asthma, chronic bronchitis (with small airway obstruction or obliteration), emphysema, and fibrosis. Current and potential exposure problems which should be investigated include fiberglass and other fibers, welding, solvents, and pesticides. The dilemma of personal vs. societal action needs to be resolved. An integrated strategy could provide quick warnings and initiation of studies for precise answers. Such strategy consists of workplace surveillance and networking of morbidity reporting, combined with observations across time which are collected in tandem with measurements of exposure. Some pilot studies and experiments are needed to perfect such a systematic program.

Chronic Disease↗

PubMedDate not supplied

Neurobehavioral and respiratory symptoms of formaldehyde and xylene exposure in histology technicians.

Disturbances of memory, mood, equilibrium, and sleep that occurred simultaneously with headache and indigestion, were experienced more frequently among women working in histology who had daily exposure to formaldehyde, xylene, and toluene than in unexposed female clerical workers working in the same hospitals. Neurobehavioral symptoms were accompanied by irritation of eyes, upper airways, and trachea. Formaldehyde exposure correlated better with neurobehavioral symptoms and with respiratory and mucous membrane symptoms than did exposure to xylene/toluene or to other agents.

Adult↗

PubMedDate not supplied

Pulmonary and neurobehavioral effects of formaldehyde exposure.

Two groups of male workers who were exposed to formaldehyde, the first group in phenol-formaldehyde-plastic foam matrix embedding of fiberglass (batt making), and the second in the fixation of tissues for histology, were studied for work-related neuro-behavioral, respiratory, and dermatological symptoms; and for pulmonary functional impairment. Forty-five male fiberglass batt makers who were studied across the initial work-shift after a holiday had average frequencies of combined neurobehavioral, respiratory, and dermatological symptoms of 17.3 for the hot areas and 14.7 for the cold areas of the process. Their symptom counts were significantly greater than those for 18 male histology technicians who averaged 7.3, and for 26 unexposed male hospital workers who averaged 4.8. During their first workshift after holidays, 58% of the batt makers had a decrease in one or more tests of pulmonary function. Nine nonsmokers had decreases more frequently than did 35 smokers; forced expiratory volume in one second FEV1.0 decreased in 16%, diffusing capacity for carbon monoxide (sb) decreased in 30%, forced expiratory flow 25-75 decreased in 16%, and forced expiratory flow) 75-85 decreased in 36%. Thirty-five percent of all 44 men had drops in FEV1.0, forced vital capacity, or in diffusing capacity (sb).

Adult↗