Environmental evaluation of workers with multiple chemical sensitivities: an industrial hygienist's view.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Patients with MCS show numerous physiological and biochemical abnormalities and are generally sicker than a control group of allergic patients. Associated with MCS are mitral valve prolapse, hypothyroidism, autoimmune thyroiditis, specific abnormalities of amino acid and essential fatty acid metabolism, and diminished activity of ESOD and EGPx. Equally prevalent among MCS patients and controls are deficiencies of magnesium and Vitamin B6. Since patients with MCS feel sick almost all of the time, it is likely that some of these abnormalities contribute to their general level of ill health, if not to their sensitivities. It is also possible that these various abnormalities are caused by some unidentified fundamental metabolic or neuroendocrine disturbance that is common to states of hypersensitivity. A provocative finding is the high frequency with which impaired anti-oxidant levels were detected. Erythrocyte activity of SOD was low in 89% and EGPx was low in 48% of MCS patients. Furthermore, 41% showed impaired excretion of essential amino acids, despite a high protein diet, and leucocyte vitamin C was low in the 5 patients not taking vitamin C supplements. Anti-oxidant deficiences may certainly contribute to hypersensitivity to environmental pollutants and toxic chemicals. In fact, treatment with anti-oxidants, including selenium, vitamin C, copper, zinc, and sulfur-containing amino acids was associated with major clinical improvement in 14 (25%) of the patients in the MCS group and with limited relief of symptoms in another 10 (18%). In all patients in whom ESOD or EGPx were repeated, improvement in levels was observed following treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
The difficult task of managing patients with MCS requires a multidisciplinary effort involving the occupational medicine physician, social worker, occupational therapist, physical therapist, psychologist, vocational rehabilitation specialist, industrial hygienist, and other involved professionals. Important objectives of management include complete review of the history and clinical findings, appropriate choice of diagnostic tests, search for additional exposure information, emphasis of "well" behavior, health education of the patient and prevention of further illness. Because of the chronic nature of MCS and the difficulty many patients have in coping with MCS, pharmacologic and psychologic interventions should be considered. Interaction of the clinic with the patients employer, insurance carrier, or attorney must be carefully planned and communicated only after receiving the patient's informed consent. Patient education should include general principles of toxicology, industrial hygiene measures to reduce hazardous exposures, factors which may aggravate the illness, and resources available to obtain further information and assistance.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Because no information exists on the prevalence of chemical sensitivity syndromes such as multiple chemical sensitivities, a questionnaire for use in population studies was developed and tested to assess the presence or absence of chemical sensitivity. Seven hundred five individuals attending clinics answered a questionnaire asking whether each of 122 common substances caused symptoms. Results showed that patients with multiple chemical sensitivities and asthma had average total scores that were significantly different from each other and from those of each of the other diagnostic categories. Higher total scores were also reported by female patients. The instrument described here may facilitate meaningful prevalence studies of multiple chemical sensitivities. It will also allow study of chemically induced symptoms in other conditions such as asthma.
Several different meanings have been attached to the term "chemical sensitivity" by those who use it. Feeling ill from odors is a symptom reported by approximately one-third of the population. The syndrome of chemical sensitivity, frequently called "Multiple Chemical Sensitivity" or "MCS" has been the subject of three federally-sponsored workshops; at least five different case definitions for research on MCS have been proposed. In contrast, the hypothesis that chemical sensitivity may be a mechanism for disease posits that a broad spectrum of "recognized" chronic illnesses, ranging from asthma and migraine to depression and chronic fatigue, may be the consequence of environmental chemical exposures. According to this theory, a two-step process occurs: (1) an initial salient exposure event(s) (for example, a one-time, intermittent, or continuous exposure to pesticides, solvents, or air contaminants in a sick building) interacts with a susceptible individual, causing loss of tolerance for everyday, low level chemical inhalants (car exhaust, fragrances, cleaning agents), as well as for foods, drugs, alcohol, and caffeine; (2) thereafter, such common, formerly well-tolerated substances trigger symptoms, thus perpetuating illness. "Masking" (acclimatization, apposition, and addiction) may hide these exposure-symptom relationships, thus obfuscating the environmental etiology of the illness. Accumulating clinical observations lend credence to a view of chemical sensitivity as an emerging theory of disease causation and underscore the need for its testing in a rational, scientific manner. While chemical sensitivity may be the consequence of chemical exposure, the term "toxicant-induced loss of tolerance" more fully describes the two-step process under scrutiny.
One hundred twelve individuals who reported onset of multiple chemical sensitivity following well-documented exposure to either (1) a cholinesterase-inhibiting organophosphate or carbamate pesticide or (2) remodeling of a building completed mail-out/mail-back questionnaires concerning their exposure, symptoms, sensitivity to ingestants and inhalants, utilization of health-care resources, and impact of their illness on lifestyle. It was hypothesized that if multiple chemical sensitivity resulted from neurotoxic exposure, then organophosphate-exposed respondents should report greater severity of illness resulting from the relatively greater neurotoxicity of this class of chemicals. Pesticide-exposed and remodeling-exposed multiple chemical sensitivity groups reported similar patterns of symptoms and identified similar inhalants and ingestants as triggers for their symptoms; these results suggested a common mechanism (biological and/or psychological) for their conditions. The pesticide-exposed group, however, reported significantly greater symptom severity than did the remodeling-exposed group, especially for neuromuscular, affective, airway, gastrointestinal, and cardiac symptoms. These findings provide evidence for (1) a possible biological basis for multiple chemical sensitivity and (2) a distinct pathophysiology or final common pathway for the condition that, while as yet undefined, appears to be shared by these two groups. Although subjective multisystem health complaints characterize both multiple chemical sensitivity and somatoform disorder, features of this multiple chemical sensitivity sample were inconsistent with somatoform disorder, i.e., onset after 30 y of age in 83%, the predominance of severe cognitive symptoms, and attributions of environmental causation. No group differences were found with respect to lifestyle impact. Eighty-one percent of respondents said they had been working full-time at the time they were exposed, yet at the time of the survey (on average, 7.7 y post exposure) only 12.5% were working full-time. The majority said they had quit their jobs, changed jobs, or changed careers because of their illness. Approximately 40% reported that they had consulted 10 or more medical practitioners. The persistent, disabling neuropsychological symptoms reported by these multiple chemical sensitivity groups are strikingly similar to those reported among individuals exposed occupationally to pesticides and solvents. These parallel findings suggest that the types and levels of exposures associated with extermination and remodeling may not be inconsequential, at least for a subset of the population. Further studies from a variety of perspectives, including human challenge studies and the development of animal models, are needed to define the pathophysiological and psychological mechanisms underlying this costly condition.
Dr. Proctor summarizes the current research literature describing Gulf War (GW) veterans' health issues, particularly as they pertain to chemical sensitivity (CS) and multiple chemical sensitivity (MCS) syndrome. In several studies of GW veterans, using differing criteria and varying assessment measures for CS and MCS, the prevalence rates for CS are reported to be 36-86% in Department of Veterans' Affairs patient populations and 0.8-20% in general cohorts of GW veterans. The rates of MCS are 2-6%. Targeted research is needed to adequately evaluate GW veterans' health concerns and MCS.
Explore the source record for details and available documents.
Toxicology has two goals. The first is to identify and characterize the adverse effects that can be produced in biological systems by exposure to chemicals and the second is to use this information to predict the type and severity of responses in other species and exposure situations. The tools that the toxicologist uses to detect and describe the adverse effects of chemical exposure include the traditional acute, subchronic, and chronic studies in animals plus a variety of special studies designed to demonstrate specific organ damage, reproductive and teratogenic effects, neurotoxicity, immunotoxicity, genotoxicity, and other responses. These are often supplemented with studies of the kinetics and the mechanism of action and more recently with studies designed to elucidate the molecular basis for cancer and other effects. Theses studies together with the information on exposure provide the basis for subsequent toxicologic predictions. Although general effects such as weight loss and mortality are included in toxicity protocols, most of the toxicology tests are related to specific end-organ toxicity or to mechanism or behavioral studies. We do not have animal protocols to study individually the subjective symptoms described for multiple chemical sensitivity, such as depression, fatigue, headache, and memory loss, and our tests lack sufficient specificity to evaluate a syndrome which is composed primarily of such symptoms. Since all chemicals can produce adverse effects under some conditions of exposure, toxicologic predictions are most useful when they specify both the type of adverse effect anticipated and the dose required to produce the effect. Multiple chemical sensitivity does not appear to consistently involve specific chemicals or specific adverse effects and the effects observed are reported to lack evidence of a threshold and to occur at extremely low levels. It is difficult to include these parameters in any reasonable toxicologic prediction relating cause and response in multiple chemical sensitivity or similar conditions.
The multiple chemical sensitivities syndrome (MCS) and other chronic syndromes causing fatigue, headache and other protean CNS symptoms without observable signs, are proposed to result from hypoxia/hypercapnia (H/H) due to disturbed breathing. The concept is explained in terms of sleep apnea (SA), although H/H could result from causes other than SA. Reasons for considering this etiologic linkage are as follows: 1. MCS symptoms resemble those of SA. 2. The only physical signs associated with MCS (upper airway inflammation and obstruction) can aggravate SA. 3. The only neuropsychiatric finding common among MCS symptomatics, reduced verbal recall, is associated with SA. 4. Many MCS symptomatics attribute onset of their condition to a pesticide or solvent exposure. Solvent neurotoxicity may cause cacosmia, a symptom of MCS and SA. 5. Improved upper airway patency, a first-line therapy in SA, may improve symptoms in some MCS-like conditions. Implications for diagnosis and treatment of MCS are discussed.
More than 68000 of the 700000 veterans of the Gulf War have become members of the Veteran Affairs' Gulf War Registry. In 1995, we undertook a questionnaire study of the symptoms and medical histories reported by a randomly selected subsample of 1935 of these veterans to characterize their complaints. All results reported were based on questionnaire responses without face-to-face evaluation or physical examinations. Inasmuch as initial registry symptoms overlapped those of Chronic Fatigue Syndrome and Multiple Chemical Sensitivities, we also included standard questions for these syndromes in the questionnaire. A total of 1161 (60%) individuals responded, and there were no major demographic biases; therefore, 15.7% of registry veterans qualified for Chronic Fatigue Syndrome in accordance with the 1994 Centers for Disease Control definition. In addition, 13.1% qualified for multiple chemical sensitivities in accordance with a widely used definition, and 3.3% of the respondents had both conditions. There were no effects of gender, race, branch, duty status (active or reserve), or rank, although Multiple Chemical Sensitivities was somewhat more prevalent in women and African Americans. The data gleaned in this study suggested that the unexplained symptom syndromes of Chronic Fatigue and Multiple Chemical Sensitivities may characterize an appreciable portion of the complaints of those who volunteered for the Veterans Affairs' Gulf War Registry, and further investigation is warranted.
Some believe that an abnormal immunoregulatory response based on environmental damage to T cells is fundamental to the production of symptoms in patients with alleged "multiple chemical sensitivity" and/or "environmental illness." According to this theory stimulation of T cells or T cell phenotypic subsets by environmental chemicals results in release of cytokines that can effect appropriate target cells of multiple organ systems, resulting in a wide range of symptoms. This concept is reinforced by frequent media reporting of pollution incidents and environmental disasters plus continued isolated reports of immunologic abnormalities in patients with various forms of alleged environmental illness, multiple chemical sensitivities, or other related syndromes. These include reports of slight perturbations in quantity and function of immunoglobulins, complement and its components, B cells, natural killer cells, T cells, phenotypic T cell subsets, and helper suppressor T cell ratios. There are also reports of increased or decreased interleukin levels including IL-1 and IL-2 or their receptors (IL-2R) in these patients. Such assays are not infrequently performed even though there is no evidence for their diagnostic efficacy in these alleged conditions. It is reasonable, however, to anticipate that with the wide development of assays for many of the interleukins and their receptors, these assays may become important in the future diagnosis of many autoimmune, allergic, neoplastic, and infectious diseases. At this time, however, the induction of environmental illness or multiple chemical sensitivity by exposure to trace levels of environmental "immunotoxins" is unproven and remains a matter of speculation. The reproducibility of immunologic test abnormalities reported under these conditions has not been documented, and the data have often not been analyzed statistically. Appropriate controls also have not usually been employed, nor have control values been provided in many cases. Without consideration of these factors, a patient might be erroneously diagnosed as having some form of "immune dysregulation," "environmental immune dysfunction," or "immunotoxic" syndrome on the basis of only a single panel of cellular immunologic profiles or related immunologic tests illustrating slight deviations from the norm and in the absence of overt disease on physical examination. Consideration must also be given to an understanding of biologic variability and diurnal variations in lymphoid cell numbers in interpreting cellular immunologic profiles. For example, the necessity for age and sex-matched controls, test reproducibility, quantitative versus functional assays, and the significance of major versus minor deviations from the norm must be appreciated. In addition, many other conditions can effect immunologic tests, such as medications, psychologic factors, cigarette smoking, and the presence of concurrent disease, including minor viral infections. All of these variables should be appreciated in test interpretation. Certain clinical indications for analysis of cellular components of the immune system, using flow cytometry, have been provided as guidelines although they are by no means accepted by all groups due to their current incomplete evaluation by the clinical immunology community. These suggested indications are discussed. In this article, attempts are made to outline the various quantitative and functional tests used to assess the immune system, with emphasis on "biomarker" tests to detect possible immune system "damage." Dangers involved in attempting to make clinical evaluations based on results of isolated in vitro assessment of quantity or function of immune system cellular and humoral components without considering the results of a good medical history and physical examination, the many pitfalls involved in the tests, and the many confounding variables that affect the tests are emphasized, as well as the need for proper controls...