The usual culprit is A. fumigatus, a fungus that grows in soil, decaying vegetation, food, water, and/ or dust. Other fungi, including Penicillium, Helminthosporium, Curvularia, and Candida, may cause a similar disease. Sensitization to the fungus leads to an inflammatory response in the lungs and airways, which includes eosinophil infiltration and increased mucus production. Eventually, bronchiectasis and pulmonary fibrosis can occur. Symptoms include wheezing, shortness of breath, cough productive of brownish mucus, fever, and malaise. Changes observed in chest radiographs are consistent with pneumonia. Laboratory studies have revealed high levels of Aspergillus-specific IgE and elevated peripheral blood eosinophils. Aspergillus skin testing reveals sensitization, but the test is also positive in patients with a simple allergy to Aspergillus. Treatment for ABPA includes corticosteroids and antifungal agents. Allergic fungal sinusitis is a disease that is pathologically similar to ABPA, but the sites of inflammation are the paranasal sinuses. Other features include nasal polyposis, nasal and sinus accumulation of fungal debris and allergic mucin, and crust formation . Cultures from the sinuses yield Aspergillus, although this is not pathognomonic, nor is the lack of positive Aspergillus cultures enough to rule out AFS. It is estimated that approx 5% of all patients with chronic rhinosinusitis have AFS. It is more common in atopic patients who have a diagnosis of allergic rhinitis and who test positive to one or more fungal allergens. AFS primarily affects young adults,vertical rack and most cases are geographically distributed in temperate areas with high humidity. Aside from Aspergillus, AFS can be caused by dematiaceous fungi, including Bipolaris, Curvularia, Exserohilum, Drechslera, Alternaria, Helminthosporium, and Fusarium. There is controversy regarding whether AFS is an infectious or allergic disease.

The fact that most patients with AFS have positive skin test and radio allergosorbent test to fungal allergens, as well as the prominent incidence of atopy in patients with AFS, support an allergic component to this disease. Eosinophils also play a significant role in AFS, and ECP levels were significantly higher in the mucin of patients with AFS compared with control patients . Criteria for diagnosis of AFS include radiographical evidence of sinusitis, positive fungal stain or culture from the sinus at time of surgery, presence of allergic mucin, absence of fungal invasion, and absence of contributory factors such as immuno deficiencies or diabetes mellitus . Differential diagnoses of AFS include saprophytic fungal growth, fungus balls of the sinuses, eosinophilic mucin sinusitis, and invasive fungal sinusitis. Hypersensitivity pneumonitis is another respiratory disease that is probably caused by microbes, but it is primarily an allergic disease. Hypersensitivity pneumonitis frequently occurs as occupational asthma, and several etiological agents have been cited. Examples of hypersensitivity pneumonitis and their suspected source include Farmer’s lung , bird fancier’s lung , pigeon breeder’s disease , hen worker’s lung , bagassosis , mushroom worker’s lung , air conditioner lung , cork worker’s lung , malt worker’s lung , sequoiosis , and woodworker’s lung . Symptoms include fever, chills, cough, and respiratory distress occurring 4 to 8 h after re-exposure to the inciting agent. If prolonged exposure is present, then the disease progresses into a chronic form and fibrosis develops, eventually leading to respiratory failure. Diagnosis is primarily based on clinical features, but it is supported by identification of the source agent, presence of specific antibodies in blood, chest radiography, pulmonary function tests, and lung biopsy. Treatment is based on avoidance and the use of corticosteroids. Therefore, it is important that individual patients be examined, including vigorous review of medical histories, physical examinations, and appropriate diagnostic testing to confirm and establish diagnosis and begin appropriate therapy.

We are continuously exposed to a wide variety of environmental pollutants, and many of them individually have been shown to have detrimental effects on health and development in experimental animals. Fewer studies exist for humans, and the results are not always consistent. This is not unexpected, however, because almost all current research neglects that humans are exposed to a myriad of environmental pollutants and that interactions between compounds may be responsible for the various symptoms and diseases that have reportedly increased in incidence in recent decades. Certain VOCs, formaldehyde, phthalates, and possibly OPs and carbamate pesticides have all been linked to lower respiratory symptoms in humans. Not only OCs, but also OP compounds, may induce subtle neurodevelopmental defects. Similarly to certain phthalates, the major DDT metabolite, p,p’-DDE, has been shown to be a potent anti-androgen in vitro and in vivo . Gestational exposure to p,p’-DDE resulted in reduced anogenital distance at birth and retention of thoracic nipples on postnatal day 13, but it did not decrease testosterone levels. Similarly, exposure to TCDD and certain PCBs can cause developmental toxicity that is manifest particularly in the male reproductive system . Conversely, o,p’-DDT, a minor component of technical grade DDT, and some DDT metabolites exhibit estrogenic activity, as do some hydroxylated PCB metabolites, whereas other PCBs and their metabolites act as anti-estrogens . This indicates a substantial potential for interactions among this large variety of compounds. Associations with decreased semen quality have been suggested not only for certain phthalates but also for PCBs overall and/or individual PCB congeners and their metabolites , p,p’-DDE , and OP pesticides . Results from an exploratory analysis suggest a greater than additive interaction between MBzP and MBP and PCB-153 and CYP450-inducing PCBs . It was proposed that this interaction could result from the inhibition of UDP-glucuronosyl transferase by hydroxylated PCBs, which results in greater amounts of free phthalate monoesters, believed to be the main biologically active metabolites. Unfortunately, neither OH-PCBs nor the ratio of free vs glucuronidated phthalate monoesters was determined. There have been few attempts to address the interaction of mixtures of compounds at physiologically relevant concentrations.

A notable exception is the pioneering work by Kortenkamp and colleagues. For example, they showed that a mixture of the OCs, o,p’- DDT, p,p’-DDT, p,p’-DDE, and β-hexachlorocyclohexane exhibited combination effects on MCF-7 human breast cancer cell proliferation when each of the components was used at concentrations at or below their respective no-observed effect concentrations . Similar results were obtained with combinations of up to 12 estrogenic chemicals in the yeast estrogen screen assays . Generally, the concentration addition model provided excellent predictions of the observed effects, whereas the independent action model, for the most part, did not. However, there were indications that cytotoxic or growth inhibitory effects of compounds included in mixtures might compromise the ability of the model to predict combination effects . The model ofconcentration addition was also found to accurately predict the effects of certain binary mixtures of environmental estrogens in vivo, using juvenile rainbow trout as the animal model and vitellogin induction as the measured end point . These findings “put into sharp relief the limitations of the traditional focus on single agent effects during hazard and risk assessments” , not only of the endocrine-disrupting chemicals this comment referenced but of many other environmental toxicants. Organic matter, such as proteins derived from living organisms, or toxins emitted by living organisms can also be associated with respiratory diseases. Combinations of aero-allergens can result in chronic allergic illnesses, including allergic rhinoconjunctivitis, sinusitis, and asthma. Mycotoxins released from fungi have not been demonstrated to cause human illness,bud drying rack although in vitro studies have demonstrated numerous cellular effects. Further research needs to be performed to characterize whether or not clinical effects of mycotoxins exist. SBS has been described since 1982, but there are no consistent data showing a common cause for the myriad of symptoms described. We do know that the symptoms are nonspecific and occur in more than one person in the same building and that multiple agents, as described earlier, have been cited as etiological factors. In addition to toxins, chemicals, and bioaerosols, there may be a major psychological component to SBS. We need the concerted effort of scientists from many different disciplines—particularly from informatics—for the identification of biological and nonbiological toxicants and the unraveling of their contribution to health effects in humans and wildlife. This should finally bring the power of computers to bear on the inordinate complexity of interactions among environmental pollutants as well as the interactions between pollutants and the organisms they affect.Mosquito survival status was examined at 24-hour post-exposure, where the survived and dead mosquitoes were collected and preserved at -20˚C prior to molecular analysis. Percentage mortality was calculated for both indoor and outdoor F1 mosquitoes.The involvement of oxidase resistance mechanism in pyrethroid resistance was determined by pre-exposing test populations to the oxidase inhibitor; Piperonyl butoxide synergist . Briefly, unfed females aged 3–5 days were pre-exposed to 4% PBO impregnated test papers for one hour. After pre-exposure to PBO, the mosquitoes were immediately exposed to each of the three pyrethroids separately for another hour. One batch of 25 females was only exposed to 4% PBO without insecticide asa control. Mosquitoes were transferred to holding tubes and supplied with 10% sugar solution. Mortality was recorded after 24 hour recovery period.

Insecticide resistance intensity testing to deltamethrin was determined by using CDC bottle bio-assay with serial dosages.The bottles were coated in batches for each working concentration, to which mosquitoes were exposed as per the CDC procedure guide MR4. The number of knocked-down mosquitoes was recorded every 10 minutes until either all mosquitoes in the test bottles were dead or it reached 1 hour after the start of the experiment. Mosquitoes were transferred to holding cups and fed on 10% sucrose solution. Mortality was recorded after 24-hours.This study set out to determine the level of insecticide resistance of Anopheles mosquito species between populations found resting indoors and those resting outdoors. Generally, high phenotypic, physiological resistance was observed in the progeny of indoor resting malaria mosquitoes than the outdoor resting vectors. In the lowland sites of Kisian , An. arabiensis was the most abundant malaria vector compared to its sibling species An. gambiae s.s. whereas in Kimaeti , the dominant species was An. gambiae s.s. similar to earlier reports . The lowlands tend to have high temperatures and low humidity which favour the more resilient An arabiensis whereas in the highlands, there are low temperatures and high relative humidity which favour An gambiae. The indoor population recorded high phenotypic resistance to pyrethroids than outdoors. The phenotypic insecticide resistance to pyrethroids in An. gambiae s.l. is widespread in Western Kenya evident in previous studies. The resistance to pyrethroids by An. funestus was observed and has as well been reported before. These regions of Western Kenya have been reported to have increasing resistance to pyrethroids which are the public health approved insecticides for use in LLINs. There was 100% susceptibility to malathion of mosquitoes just as similar studies have shown in Ghana. Synergist PBO pre-exposure restored susceptibility for both indoor and outdoor resting mosquitoes, revealing the role of detoxifying metabolic enzymes in the insecticide resistance in these regions. This means, therefore, that there are more factors at play contributing to the insecticide resistance present in Western Kenya similar to studies before. Increasing the concentration of the deltamethrin in CDC bottle assays restored susceptibility to 100% suggesting that the continuous exposure to the current dosage in LLINs and possible interaction with non-lethal doses in agricultural chemicals could have been at play to contribute to the development of resistance to pyrethroids as previously demonstrated in indoor resting and outdoor resting malaria mosquitoes. The result showed moderate intensity insecticide resistance since the mosquitoes succumbed to the highest concentration according to the WHO test procedures for insecticide resistance monitoring in malaria vectors. The buildup of the phenotypic resistance which was higher in indoor resting mosquitoes compared to the outdoor resting counterparts might be threatening current insecticide-based malaria control interventions as suggested by prior studies. The presence of resistance-associated point mutations was more in indoor resting mosquitoes than their outdoor resting counterparts. This can be attributed to the adaptations from selection pressures due to constant exposure to insecticide-based interventions such as LLINs and the extensive chemicals used in the tobacco farms in Kimaeti. The study also detected, even though in lower frequencies, a significant proportion of the vgsc-1014S and 1014F in An. arabiensis a phenomenon that has been previously reported. This is in line with studies that have shown the occurrence of more than one kdr associated point mutation within a population of An. gambiae s.l. already reported previously.