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'Sensitivity syndromes' related to radiation exposures.

The primary health effects of radiation are traditionally believed to result from cellular genetic damage. These effects are believed to result in a statistically detectable increase in the induction of cancer in exposed populations. A significant number of residents of areas affected by the Chernobyl disaster and workers involved in the clean-up ('liquidators') have reported debilitating physical illnesses that cannot be easily explained by a genetic effect. This paper presents results of a literature search that strongly suggests that a previously unrecognized neural pathway may be responsible for the induction of these debilities. In addition, a common link between radiation and chemical sensitivity syndromes may now be identified.

Humans↗

Patient statement: chemically sensitive.

There are three areas of my experience with chemical sensitivity that may interest you. The first is the onset of this condition and what happened to me over time as I became chemically sensitive in my work place. The second is my experience with the "medical community." The third is the effect chemical sensitivity has had on my career.

Female↗

Controlled exposures to volatile organic compounds in sensitive groups.

Sensitivities to chemicals are characterized by symptoms in multiple organ systems in response to low-level chemical exposures. This paper reviews studies of controlled exposures to odorants and to mixtures of volatile organic compounds. Sensitive subgroups include subjects who met Cullen's 1987 criteria for multiple chemical sensitivity (MCS), Gulf War veterans with chronic fatigue syndrome and chemical sensitivity (CFS/CS), and subjects with specific self-reported sensitivities to methyl terbutyl ether (MTBE) in gasoline (MTBE-sensitive). All studies include comparison of age- and sex-matched healthy controls. Studies of olfaction did not support unusual sensitivity, defined as lower odor thresholds, among MCS subjects; however, a dose-response pattern of symptoms was observed in response to suprathreshold concentrations of phenyl ethyl alcohol. In blinded, controlled exposures to clean air, gasoline, gasoline/11% MTBE, and gasoline/15% MTBE, a threshold effect was observed with MTBE-sensitive subjects reporting significantly increased symptoms to gasoline/15% MTBE exposure. Autonomic arousal (heart and respiration rate; end-tidal CO2) in response to odor of chemical mixtures may mediate symptoms for subjects with generalized chemical sensitivities, but not for those whose sensitivities are confined to specific chemicals. For example, Gulf War veterans with CFS/CS experienced reduced end-tidal CO2 when exposed to diesel fumes, while exposure to MTBE did not produce any psychophysiologic changes in MTBE-sensitive subjects. Controlled olfactory and exposure studies reveal that significant responses can be observed in chemically sensitive subjects even when de-adaptation has not occurred. However, these studies suggest that symptoms are not necessarily accompanied by changes in physiologic arousal. Subject characteristics play a critical role in outcomes.

Adult↗

Subjective ratings of odorants by women with chemical sensitivity.

The purpose of the present study was to investigate whether women with chemical sensitivity rated the intensity and pleasantness of three odorants [peppermint, vanilla, and propylene glycol (PG)] and odorless room air differently than women without chemical sensitivity. The ratings of the experimental group (women with self-reported chemical sensitivity and no history of sexual abuse) were compared to those of two control groups who did not report chemical sensitivity [sexually abused (SA) women and healthy women without sexual abuse history]. All subjects were exposed to odorants and odorless control stimuli once a week for 3 consecutive weeks. Our findings indicate that women with chemical sensitivity perceive odorants as neither more or less intense nor more or less pleasant than women without chemical sensitivity. Moreover, the control women without sexual abuse outperformed the women in the other two groups by correctly identifying the target bottle containing the odorant. These findings suggest that perception of odorants alone is unlikely to account for the symptoms associated with chemical sensitivity. These findings, along with those of Doty et al. (1988), support the notion that olfactory-sensory function does not differ between individuals with and without chemical sensitivity.

Adult↗

Chemical sensitivity and the immune system: a paradigm to approach potential immune involvement.

This paper approaches the issue of chemical sensitivity and the immune system though a consideration of established environmentally-induced immune alterations which have particular relevance to the broader topic of chemical sensitivity. Additionally, the report discusses the potential problems associated with prior narrow evaluation strategies for the assessment of environmentally-induced inflammation. A combined approach to assessment drawing upon biomarkers of both the immune and neurological systems is suggested. Such an approach recognizes the key roles which mediators of these two systems play in facilitating host inflammatory responses. The paper concludes with a discussion of the types of specific immune alterations which, from a mechanistic perspective, are likely to be involved with any linkage of chemical sensitivity to the immune system.

Environmental Exposure↗

Neurotoxicity in single photon emission computed tomography brain scans of patients reporting chemical sensitivities.

The subset of patients reporting chemical sensitivity with neurocognitive complaints usually exhibits specific abnormalities of brain metabolism consistent with neurotoxicity, on imaging with single photon emission computed tomography (SPECT). These recurrent neurotoxic patterns are characterized by a mismatch in tracer uptake between early- and late-phase imaging, multiple hot and cold foci throughout the cortex, temporal asymmetry and increased tracer uptake into the soft tissues and, sometimes, the basal ganglia. Previous studies confirm these neurotoxic findings in patients with neurotoxic chemical exposures and breast implants. Affective processes such as depression do not, alone, show this pattern. These abnormalities in SPECT images correlate with documented neurocognitive impairment. Controlled challenges to ambient chemicals can induce profound neurotoxic changes seen on SPECT imaging in chemically sensitive patients. Detoxification treatment techniques frequently produce significant improvement on brain SPECT brain imaging in these patients. Neurotoxicity appears to be characteristic in many cases of chemical sensitivity.

Brain↗

Mechanisms of allergy and chemical sensitivity.

Allergy and chemical sensitivity are closely related disorders in which environmental exposures produce inflammatory reactions. For allergy, environmental proteins bind to IgE antibody on mast cells leading to the release of inflammatory mediators. In chemical sensitivity, low molecular weight chemicals bind to chemoreceptors on sensory nerve C-fibers leading to the release of inflammatory mediators. Clinical manifestations are similar in the two conditions. The overlap between the two conditions has a basis in mechanism, so the similarity of clinical manifestations and high percentage of individuals with both conditions may have a biological basis. Chronic exposures can lead to adaptation phenomena. Depression has been associated with both allergy and chemical sensitivity. Both the allergic and chemical irritant responses may be subjected to conditioning so that the response is triggered by other stimuli. Evidence for conditioning is strongest for allergy. Both allergy and chemical sensitivity can be acquired in association with irritant exposures.

Adaptation, Physiological↗

Evolving concepts of chemical sensitivity.

Chemical sensitivity appears to be an elusive phenomenon. Studies on individual differences in susceptibility may provide glimpses into the range of sensitivity in a population, which can be used for further study. Preliminary evidence in laboratory animals suggests the range of sensitivity to manufactured chemicals may span orders of magnitude. Determining the reasons that underlie individual differences in sensitivity is a more difficult enterprise. Conditioning of adverse physiological effects of airborne chemicals may play a vital role in the etiology of chemical sensitivity, and it provides a rigorous laboratory model by which to investigate some aspects of this elusive phenomenon.

Animals↗

Physiologic and symptomatic responses to low-level substances in individuals with and without chemical sensitivities: a randomized controlled blinded pilot booth study.

We conducted a pilot study using a randomized, single-blind, placebo-controlled exposure among 10 individuals with and 7 without reported chemical sensitivities in a dedicated testing chamber. Objectives of the study were to explore the length of the adaptation period to obtain stable readings, evaluate responses to different substances, and measure the level and type of symptomatic and physiologic reactions to low-level exposures. Reported and observed symptoms, electrodermal response, heart rate, skin temperature, surface electromyogram, respiratory rate, contrast sensitivity, and the Brown-Peterson cognitive test were used and compared between cases and controls and between test substances (glue, body wash solution, dryer sheet) and control substances (unscented shampoo and clean air). Subjects with chemical sensitivities (cases) took longer to adapt to baseline protocols than did controls. After adaptation, despite small study numbers, cases displayed statistically significant responses (all measures, p < 0.02) in tonic electrodermal response to test substances compared with controls and compared with the control substance. Symptoms were also higher in cases than in controls for the body wash solution (p = 0.05) and dryer sheets (p = 0.02). Test-retest showed good agreement for both symptoms and tonic electrodermal responses (McNemar's test, p = 0.32 and p = 0.33, respectively). Outside of skin conductance, other measures had no consistent patterns between test and control substances and between cases and controls. This study shows the importance of using an adaptation period in testing individuals with reported chemical sensitivities and, despite small numbers, raises questions about underlying mechanisms and level of reactivity to low-level chemical exposures in sensitive individuals.

Adhesives↗