Identify and briefly describe four of the six environmental factors affecting international projects

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4.1 INTRODUCTION

This chapter discusses four environmental factors or features that arise from the surroundings (i.e., illumination and temperature) and mechanical features of the workplace (i.e., noise and vibration) that could be encountered at work and affect behavior. Other examples of environmental features that could be encountered at work and may affect behavior are dangerous chemicals, radioactive materials, atmospheric pressure, and the like. These other environmental features are not discussed in this chapter.

This chapter discusses the four environmental features that can affect people in three ways: (1) health, (2) performance, and (3) comfort. The affects of these three aspects are usually combined. For example, poor health can lead to both poor performance and reduced comfort and, thus, reduced work satisfaction. Stressors, arising from illumination, temperature, noise, vibration, or any other aspect of the environment can adversely affect people when they reach a certain level, although the effect may not be apparent either to the person being affected or an observer. The ideal range for performance and comfort is narrow. Therefore, trying to adapt to conditions outside the ideal range can make people use more effort, which can lead to reduced performance and comfort; for example, a person trying to see fine details when illumination levels are too low or too high.

This chapter ends with a case study examining the lighting quantity and quality in a control room. In addition, a set of review questions are included to help you check your understanding of the material covered in this chapter.

2.11 Conclusion

Environmental factors found to associate with social status have important effects on the development, morphology, and function of various brain networks supporting language, attention, executive function, and stress responses. Whereas results may vary based on how researchers characterized SES, these findings indicate that future research integrating neuroimaging methodologies and rigorous examinations of socioeconomic factors should lead to a better understanding of the relationship between social status and brain function. To accomplish this goal, further research may also benefit from investigating the impact of mechanisms related to prenatal and genetic influences. Furthermore, better understanding the impact of social status on social interactions may provide insights into its pervasive role in multiple facets of our lives. Indeed, recent functional neuroimaging investigations suggest that one’s own social status and the social status of others shape fundamental social cognitive processes.

Understanding Environmental Factors

Environmental factors in the ICF are determinants of disabilities, coequal in significance with health conditions. Two individuals with precisely the same health condition, and impairments, may experience vastly different restrictions in the lives because of features of their physical and social environment: one may be able to be fully employed because of workplace accommodations; the other may face such significant social stigma that he or she is housebound. The presence of facilitators and barriers shape individual lives and the experience of disability. Yet, other than the easy cases of the provision of assistive technology and accommodations, or social exclusion and discrimination, we know very little about how environmental factors interact with health states to yield decrements in functioning. The ICF provides the vocabulary for describing these factors, but the science and instrumentation needed to assess and measure this impact is, at best, in its infancy.

To be sure, occupational and physical therapists have long appreciated the need for exact description of environmental impact since many of their interventions depend on it. Yet, while their knowledge about the direct or immediate physical environment of assistive technology and physical accommodations may be well developed, the impact, positive or negative, of other domains of the environment are far less so. Social attitudes, both cultural and interpersonal, clearly affect how health conditions and impairments impact people's lives, but the mechanisms underlying this impact are not at all well-known. We are even more ignorant of how macrolevel environmental changes in the form of laws and regulations, policies, and programs impact people's lives. While political activism may successfully alter our laws and policies, astonishingly, we lack the tools and indicators for identifying, let alone measuring, the impact of policy change on the lived experience of disability.

Environmental factors

Environmental factors that may trigger vitiligo remain unclear at this time. A subset of patients has been described to have ‘contact vitiligo’ or ‘occupational vitiligo.’ This describes a form of vitiligo caused by exposure to particular chemicals, typically aromatic or aliphatic derivatives of phenols and catechols. Depigmentation may be limited to areas exposed to chemicals, or it may progress from the initial site of chemical exposure to the whole body, which is consistent with NSV. Instead of being the causative agent for contact/occupational vitiligo, it is possible that chemical agents may serve as an environmental trigger for the induction of vitiligo. The precise definition of this entity remains unclear, as sufficient epidemiological studies have not been performed to investigate potential predisposing risk factors, time between exposure and onset of depigmentation in exposed areas, and time between first depigmentation and onset of generalized vitiligo.

An important feature with vitiligo is that depigmentation only occurs in patients with a predisposition to develop vitiligo. Melanocytes in pigmented skin of vitiligo patients have aberrant morphology, which suggests that they are increasingly sensitive to stress. It has also been demonstrated that melanocytes from vitiligo patients release more HSP70 in response to model stressor compound 4-TBP. Stress proteins are capable of activating dendritic cells.

Environmental factors, including nutrition and metal elements, are implicated in the pathophysiology of Alzheimer’s disease (AD). Several in vitro and in vivo data indicate a role for magnesium (Mg) in many biological and clinical aspects of AD. Mg deficiency, aside from having a negative impact on the energy production pathways required by the mitochondria to generate adenosine triphosphate, also affects many biochemical mechanisms vital for neuronal properties and synaptic plasticity, including the response of N-methyl-d-aspartate receptors to excitatory amino acids, stability, and viscosity of the cell membrane. Mg also has an action as a mild calcium antagonist, and as an antioxidant against free-radical damage of the mitochondria. Total and ionized Mg levels in plasma, as well as Mg concentrations in various tissues, were found to be decreased in AD patients and negatively associated with clinical deterioration. Chronic Mg deficiency results in excessive production of oxygen-derived free radicals and low-grade inflammation, these also being possible pathogenic factors in AD. Moreover, Mg was shown to have a role in the processing of amyloid-beta precursor protein, which plays a central role in the pathogenesis of AD. Whether Mg supplementation may help in preventing cognitive decline in the elderly remains to be demonstrated.

Environmental Influences

Environmental factors are often influential in determining the occurrence and intensity of aggressive behaviors exhibited by athletes, spectators, and others involved in sports. The list of factors thus far shown to affect people's aggression includes crowding, darkness, odors, ions, noise, colors, and temperature. Two examples will serve to demonstrate the influence of environmental factors specifically on athletic aggression.

One of the first decisions for owners of a new sports franchise is the selection of the team's colors. The choice of color is recognized as an important consideration in creating a club's image for the public and, of course, for their league opponents. In the case of black, everyone recognizes its traditional associations in the cultural West with evil, death, and generally sinister forces. Teams seeking to impress their opponents with their toughness or aggressive play, therefore, may choose black as the basic color for their uniforms. The Raiders, formerly of Los Angeles and Oakland, now of Las Vegas, are a team whose color scheme of black and silver exemplify their namesake and inform their team's and fan base's image.

An intriguing question is whether professional sports teams actually behave in ways that are consistent with the color of their uniforms. That is, are teams wearing black also “black-hearted,” so to speak? An answer was found in the penalty records of the National Football League (NFL) and the NHL.

The uniforms from both leagues were first classified as being either predominantly black, for example, the Raiders, or nonblack, for example, Miami Dolphins. An examination of league records showed that teams at or near the top of the standings in the penalty column typically wore black, including an increase in penalties when teams switched from nonblack to black uniforms (Forbes et al., 2006). This could result from the combination of referees' calling a tighter game and the players themselves giving freer rein to their aggressive urges when attired in black. As a footnote, black-uniformed teams in the NFL and NHL had the same percentage of wins as teams wearing nonblack uniforms (Forbes et al., 2006).

A second environmental question that has drawn considerable interest from researchers is the relationship between atmospheric temperature and aggression. For instance, some studies strongly support the idea that the hotter the temperatures the more violent crime occurs. Sports provided an alternative setting for testing the temperature–aggression hypothesis. The prediction that increases in interpersonal aggression accompany increases in temperature has been tested and confirmed in a number of settings, including in baseball and football. For instance, a study of NFL football penalties found that increases in temperature positively predicted increases in aggressive penalties (Craig et al., 2016).

B. Environmental Causes of Developmental Instability

Environmental factors include temperature, food, pollutants, population density, sound, light, and parasites. The diversity of environmental stresses that have been shown to cause an increase in asymmetry is probably not exclusive; many other kinds of stress might provide similar effects.

Temperatures that deviate from optimal conditions result in increased energy expenditure for stress resistance. Increased temperature differences from the normal range encountered have been shown to result in increased asymmetry in Drosophila (Beardmore, 1960), rats Rattus norvegicus (Gest et al., 1983, 1986), and a number of other organisms (review in Møller and Swaddle, 1997).

Nutritional stress has been shown to increase asymmetry in a number of different organisms under experimental conditions. For example, European nuthatches, Sitta europaea, that had a couple of feathers removed during winter, regrew these feathers more symmetrically when provided with extra food than did control birds (Nilsson, 1994). Similar results have been obtained for a wide variety of organisms (Møller and Swaddle, 1997).

Free-living organisms encounter a diverse chemical environment during development, particularly in species with external fertilization. Deviations from commonly encountered conditions result in increased developmental instability. This is the case for several different kinds of pollutants, but also for chemicals found in the food consumed by animals. For example, gray seals, Halichoerus grypus, from the Baltic had increased asymmetry in their skulls during the 1950s and 1960s (Zakharov and Yablokov, 1990), but experienced a decrease in asymmetry as the concentrations of pollutants decreased in recent decades (Zakharov et al., 1989). In a similar vein, alcohol consumption in pregnant women resulted in increased asymmetry in their children (Kieser, 1992). Further examples are discussed in Section V,A.

Increasing population density results in a reduction in the amount of nutrients available per individual, but also in energy spent on stress resistance that could otherwise be used for control of developmental processes. Several studies have shown that asymmetry and phenodeviants increase as a consequence of increased density. For example, elevated larval density of Australian sheep blowflies, Lucilia cuprina, resulted in increased asymmetry in the adult flies (Clarke and McKenzie, 1992). Similarly, although under more natural conditions, skeletal asymmetry followed population density in the small mammal cycles of the common shrew, Sorex araneus, in Siberia (Zakharov et al., 1991). A final example derives from a study of similarly aged clones of poplars, Populus americanus, planted at three different densities (Rettig et al., 1997). The effect of density on asymmetry increased linearly from a density of .167 to 2.0 plants per square meter.

Audiogenic stress may also increase asymmetry of the phenotype. Early experiments by Siegel and Smookler (1973) demonstrated that pregnant rats that were exposed to noise had pups with increased dental asymmetry. This effect has been repeated in a number of subsequent experiments on rats and other rodents (review in Møller and Swaddle, 1997).

A final example of an environmental component that can increase asymmetry is exposure to predators (Witter and Lee, 1995). Molting starlings, Sturnus vulgaris, were kept in aviaries with food provided near or away from shelter. Hence, there was no differential exposure to predators per se, but just a perceived difference in exposure. Starlings that developed their feathers while feeding at an exposed food source developed significantly greater feather asymmetry than did controls. As asymmetric individuals are more likely to fall prey to predators (Section IV), increased perceived risks of predation may actually result in increased predation, if increased morphological asymmetries give rise to reduced performance.

In conclusion, the development of an individual integrates the effects of a wide range of environmental and genetic factors that affect the stability of developmental processes. This is an advantage for the scientists because the overall effect of many different factors is added up into the phenotype, but a disadvantage because we will not obtain information on the particular factor that is causing an increase in asymmetry.

Environmental Factors

Various environmental factors also play an important role in the pathogenesis of hypertension. Obesity, elevated sodium intake, low potassium and fiber intakes, excessive alcohol consumption, decreased physical activity, and stressful home and work environments have become commonplace in many societies and strongly contribute to the development of hypertension.

Increased sodium intake is likely to be one of the chief factors in the development of hypertension. It has been observed that many isolated populations demonstrate little or no rise in blood pressure with age in contrast to more developed societies. One of the most salient and consistent differences between developed societies and these isolated populations is a very low mean sodium intake. Even within isolated populations, those with a lower intake of sodium and hence having a lower sodium:potassium excretion ratio in urinary testing, have lower blood pressures and less age-related increase in blood pressure.

Migration studies, such as that of He and colleagues (1991) among the Yi people of China, have also supported the primary role of environmental factors such as elevated sodium intake, low potassium intake, weight gain, decreased physical activity, and other lifestyle changes in the development of hypertension. However, some of the best evidence for the influence of these environmental factors in the development of hypertension has come from randomized controlled trials testing strategies for the prevention and treatment of hypertension.

Vulnerability to Drug-seeking—Environmental Factors

Environmental factors in adults, both intrinsic and extrinsic, also are important determinants of self-administration behavior, particularly during acquisition of the behavior and during reinstatement of drug-taking following extinction (Le Sage et al., 1999). Food deprivation increased drug-maintained behavior, and this generalized to different species, routes of administration, and reinforcement schedules (de la Garza and Johanson, 1987). Food restriction increased cocaine self-administration during unlimited access to cocaine during acquisition and reinstatement (Carroll et al., 1979; Carroll, 1985). Nondrug reinforcers, such as those concurrently available during acquisition and maintenance of cocaine self-administration, prevented acquisition and decreased maintenance of self-administration behavior (Carroll et al., 1989; Carroll and Lac, 1993; Carroll and Rodefer, 1993). Nondrug reinforcers in a clinical setting also reduced cocaine intake (Higgins et al., 1994). How these intrinsic and extrinsic factors interact with the allostasis model of addiction proposed here remains a challenge for future work.

Environmental events during critical periods of development can produce enduring neuroendocrinological and neurodevelopmental changes that could influence drug reward responsivity and propensity to addiction (Moyer et al., 1978; Fride and Weinstock, 1989; Henry et al., 1994). Prenatal stress has been found to have long-term effects on the activity of the dopamine system and on dopamine-related behaviors (Moyer et al., 1978; Fride and Weinstock, 1989). Moreover, there is evidence that prenatal stress increases and prolongs corticosterone secretion in response to stress (Henry et al., 1994). Self-administration of stimulants has been studied in the offspring of mothers submitted to a restraint stress procedure during the last week of pregnancy (Maccari et al., 1991; Deminière et al., 1992). These animals also were tested for locomotor reactivity to novelty and to psychostimulants, since these behaviors are characteristically enhanced in animals spontaneously predisposed to self-administration of drugs of abuse (Piazza et al., 1989). Prenatallly stressed animals had an increased and more rapid locomotor eactivity to amphetamine, particularly over the first hour of testing. Furthermore, prenatal stress influenced the propensity to develop amphetamine self-administration. While control and stressed animals did not differ during the first day of testing, animals in the prenatal stress group showed a higher intake of amphetamine on subsequent days.

Although the development of an organism presumably carries a strong genetic component, the organism's early environment has long-lasting influence. Both components shape psychobiological temperaments and are at the origin of individual differences. Moreover, both components can contribute equally to vulnerabilities for neurodegenerative processes and ultimately deleterious life events. Prenatal and postnatal events modify the activity of the HPA axis (Caldji et al., 1998; Ladd et al., 2000), and maternal glucocorticoids have a major role in the development of endocrine function in the offspring. In fact, high levels of maternal glucocorticoids during prenatal stress have marked long-term repercussions on the efficiency of the offspring's HPA negative feedback mechanisms. Thus, a modification of corticosterone secretion via changes in HPA axis activity could be a biological substrate of the long-term behavioral effects of prenatal and postnatal events that could contribute to individual differences in vulnerability to primary allostasis in the brain reward system (see above).

Environmental and Lifestyle Factors

Environmental factors affect foodborne disease trends directly via ambient temperature, or indirectly by influencing human activity. The seasonal trends of Salmonella, Campylobacter, and EHEC are well documented: the highest incidence occurring during the warmer months, reflecting the potential for greater microbial loading in the environment and in food stored at too high temperature, and people engaging in risky practices. These include, leaving food in the car too long when shopping, and activities including camping, picnicking, and barbequing, where temperature control of food is difficult to maintain. Other climate factors include heavy rainfall causing land run off carrying animal or human feces into irrigation and process water and resulting in surface contamination of vegetable and salad crops or fruit grown on the ground. Outbreaks linked to hanging fruit may be associated with contaminated irrigation, washing or cooling water, or in the use or consumption of contaminated dropped fruit. For example, the juice outbreaks due to Salmonella, E. coli O157:H7, and Cryptosporidium identified in Table 6 followed the use of dropped apples and oranges.

It is difficult to quantify the impacts of climate change on disease trends; however, modeling ambient temperatures against foodborne illness, and Salmonella incidence specifically, indicates a relationship. Descriptive approaches suggest that aboriginal Americans, and northern people in particular, are experiencing effects of climate and environmental change. However, the extent to which environmental change is affecting factors such as lifestyle and disease prevalence in wildlife compared to other factors relating to, for example, socially driven cultural change, is unclear. Some reliance on country foods (game, fish, and sea mammals) anyway results in increased risk from parasitic diseases such as Trichinella spiralis and tapeworms compared with the general population. For example, all seven outbreaks of Trichinella infection in a Canadian review were associated with meat from wild animals, and there is indication that changes to traditional food practices carry increased risk of botulism.

Botulism is an interesting case study: a disproportionate number of incidents are recorded in Alaskan and Canadian Inuit. Most Canadian cases since the 1970s involved northern people and the US data indicates that 36% of events and 38% of cases recorded between 1990 and 2000 occurred among the relatively small Alaskan population. This compares with botulism in Canada between 1917 and 1973 when most cases were of European descent and linked to home-canned foods. This reflects a decline in home canning by Europeans as commercial availability of nonseasonal products increased, and the influence of environmental and lifestyle factors on aboriginal people resulting in the consumption of improperly preserved sea products or game eaten raw, dried, or fermented. Traditional approaches to fermentation of fish-heads, fish eggs, whale fins, seal flippers, and beaver tails relied on prolonged cold fermentation by burial in permafrost cooled ground. Investigation of outbreaks in Alaskan and Canadian native people since the late 1940s found that introduction of new country foods to a community and modified fermentation practices, including the use of sealed glass jars and plastic containers were the contributing factors. Whale and seal meat have occasionally been associated with Salmonella outbreaks in aboriginal people, and although it is unclear whether the animal had Salmonella infection or presence of the pathogen resulted from contamination by seagulls.

Fish and shellfish-associated illness has a long history and is caused by diverse agents including bacteria, parasites, and viruses as well as toxins produced by algae, diatoms, and bacteria naturally occurring in the environment, particularly Vibrio species. Although reported numbers of cases and outbreaks related to seafood are relatively low (a few hundred cases annually in the US and Canada combined) the popularity of seafood, their importation from many countries, and the serious illness caused by some agents identifies these products as potentially risky. Some seafoodborne agents, including fish and shellfish toxins and Vibrio bacteria, are recognized as emerging causes of illness that are potentially influenced by environmental conditions including ambient temperature and marine pollution from coastal land run off of nutrients. These conditions contribute to toxic algal blooms (red tides) producing neurotoxins (neurotoxic shellfish poisoning, paralytic shellfish poisoning, and amnesic shellfish poisoning) and diarrhoetic toxins (diarrhoetic shellfish poisoning). Although many illnesses are mild and under reported, occasional deaths are linked to several toxins and neurotoxic illness may have long-term health impacts; an outbreak of amnesic shellfish poisoning in Canada in 1987 resulted in 107 cases, some with persistent memory loss.

Outbreaks associated with fish in the US are mostly linked to scombrotoxin (57% of fish associated outbreaks: 1983 to 1992) and ciguatoxin (19%). Scombrotoxin, which induces histamine accumulation due to naturally occurring bacteria, is linked to poor temperature control post harvesting. Ciguatera poisoning is related to dinoflagellate toxins accumulating up the food chain, and human illness is primarily linked to higher carnivores. Puffer fish poisoning, resulting from toxins produced by naturally occurring bacteria, is rare in the US and Canada and cases are usually linked to imported fish.

Historically typhoid was the most important shellfish-associated illness, but since the mid-1950s such outbreaks have virtually disappeared. Introduction of purification procedures (depuration) in the 1930s, declining typhoid in the population and introduction of stringent microbiological criteria for shellfish growing waters, along with monitoring programs, have reduced sewage-related illness. The exception is viral pathogens present in human feces, principally noroviruses, hepatitis A, and non-A, and non-B hepatitis. Introduction of rapid molecular methods to identify noroviruses has contributed to an increase in reported incidents, and indicates that they caused many gastroenteritis outbreaks (up to 50%) previously described as unknown etiology. Currently, noroviruses are estimated to account for two-thirds of all foodborne illnesses (Table 5), although the proportion linked to seafood is unknown. Interestingly, the description of self-limiting gastroenteritis 1 to 2 days after eating oysters in documented typhoid (about 2 weeks incubation) outbreaks in the nineteenth century in the US suggests viral gastroenteritis may have been common then, and was even considered a possible prodrome of typhoid.

Naturally occurring bacteria of the family Vibrionacaea, which include Vibrio, Aeromonas, and Plesiomonas species, account for most bacterial illnesses linked to seafood. Most cases are due to Vibrio species associated with filter feeding bivalve molusks such as oysters (usually eaten raw). An estimated 5000 foodborne Vibrio infections occur annually in the US (Table 5); in Canada, less than 50 isolates are reported annually, including nonfoodborne infections and infections acquired abroad. Laboratory reported Vibrio infections include toxigenic Vibrio cholerae (types O1, O139, and recently O141), and more commonly V. vulnificus (Gulf coast) and V. parahaemolyticus (commonly on the Pacific coast). Unlike toxigenic V. cholerae O1 and V. parahaemolyticus, V. vulnificus rarely causes diarrhea and is of concern because of the high mortality associated with septicemic infection in vulnerable groups. In one report of cases linked to oyster consumption in Florida between 1991 and 1994, the mortality rate was 60%. Concerns about Vibrio infections, particularly in the US Gulf States led to the development of the Cholera and Other Vibrios Surveillance System (COVISS), maintained by the Centres for Disease Control and Prevention (CDC) since the late 1980s.

The Vibrios primarily associated with human illness share tolerance for salinity (greater in the noncholera Vibrios) and are common in warm seawater including estuaries. Their reservoirs include fish, shellfish, plankton and sediment, and their complex ecology affects their persistence in the marine environment and increased prevalence in warmer months. There is potential for introduction of species into new environments via ship ballast water, the likely route for the introduction of V. cholerae O1 El Tor (Latin American biotype) into the northern Gulf of Mexico during the Latin American epidemic in the early 1990s. A similar mechanism may also play a role in the dispersal of toxic algae.