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S C Rowat

Publications and source records attributed to S C Rowat.

3 recordsLinked to original sources

Incinerator toxic emissions: a brief summary of human health effects with a note on regulatory control.

Toxic emissions from municipal solid waste (MSW) and hazardous waste incineration are discussed, with reference to recent reviews and to government standards and controls. Studies of known effects of aromatic hydrocarbons, other organics, dioxins, metals, and gases, on fish, soils, plants, and particularly humans are briefly reviewed. A summary of potential problems with existing and proposed incineration is developed, including: (1) lack of toxicity data on unidentified organic emissions; (2) unavoidability of hazardous metal emissions as particles and volatiles; (3) inefficient stack operation resulting in unknown amounts of increased emissions; (4) formation in the stack of highly toxic dioxins and furans, especially under inefficient conditions, and their build-up in the environment and in human tissue; (5) the lack of adequate disposal techniques for incinerator fly ash and wash-water; (6) the contribution of emitted gases such as NO2, SO2 and HCL to smog, acid rain, and the formation of ozone, and the deleterious effects of these on human respiratory systems; (7) the effects and build-up in human tissue of other emitted organics such as benzene, toluene, polychlorinated biphenyls (PCBs), alkanes, alcohols, and phenols; (8) lack of pollution-control and real-time efficiency-monitoring equipment in existing installations. The inability of regulatory bodies historically to ensure compliance with emission standards is discussed, and a concluding opinion is offered that it is inadvisable to engage in new incinerator construction with present knowledge and conditions.

Air Pollutants↗

Paraoxonase/MCS.

Explore the source record for details and available documents.

Aryldialkylphosphatase↗

Integrated defense system overlaps as a disease model: with examples for multiple chemical sensitivity.

The central nervous, immune, and endocrine systems communicate through multiple common messengers. Over evolutionary time, what may be termed integrated defense system(s) (IDS) have developed to coordinate these communications for specific contexts; these include the stress response, acute-phase response, nonspecific immune response, immune response to antigen, kindling, tolerance, time-dependent sensitization, neurogenic switching, and traumatic dissociation (TD). These IDSs are described and their overlap is examined. Three models of disease production are generated: damage, in which IDSs function incorrectly; inadequate/inappropriate, in which IDS response is outstripped by a changing context; and evolving/learning, in which the IDS learned response to a context is deemed pathologic. Mechanisms of multiple chemical sensitivity (MCS) are developed from several IDS disease models. Model 1A is pesticide damage to the central nervous system, overlapping with body chemical burdens, TD, and chronic zinc deficiency; model 1B is benzene disruption of interleukin-1, overlapping with childhood developmental windows and hapten-antigenic spreading; and model 1C is autoimmunity to immunoglobulin-G (IgG), overlapping with spreading to other IgG-inducers, sudden spreading of inciters, and food-contaminating chemicals. Model 2A is chemical and stress overload, including comparison with the susceptibility/sensitization/triggering/spreading model; model 2B is genetic mercury allergy, overlapping with: heavy metals/zinc displacement and childhood/gestational mercury exposures; and model 3 is MCS as evolution and learning. Remarks are offered on current MCS research. Problems with clinical measurement are suggested on the basis of IDS models. Large-sample patient self-report epidemiology is described as an alternative or addition to clinical biomarker and animal testing.

Acute-Phase Reaction↗