Friday, June 27, 2014
Monday, May 12, 2014
Quote of the Day
“In the age of technology there is constant access to vast amounts of information. The basket overflows; people get overwhelmed; the eye of the storm is not so much what goes on in the world, it is the confusion of how to think, feel, digest, and react to what goes on.”
― Criss Jami, Venus in Arms
― Criss Jami, Venus in Arms
Friday, May 9, 2014
Quote of the Day
"I mean, is ‘fat’ really the worst thing a human being can be? Is ‘fat’ worse than ‘vindictive’, ‘jealous’, ‘shallow’, ‘vain’, ‘boring’ or ‘cruel’? Not to me; but then, you might retort, what do I know about the pressure to be skinny? I’m not in the business of being judged on my looks, what with being a writer and earning my living by using my brain…"
~ J.K. Rowling
~ J.K. Rowling
Wednesday, May 7, 2014
Air Pollution: Hazardous and Toxic Substances
My upper Midwestern home may not be the cleanest city in the world
when it comes to environmental health issues, but it certainly could be
considered one of the cleanest cities in the upper Midwest. Researching heavy metal toxicity and
hazardous substance health issues for my current environmental health course did not readily turn up anything outstanding. Turning
to the Environmental Protection Agency’s “My Environment” web page helped to
narrow down health risks. Under the My
Health section is a list of the most common found hazardous substances and
their environmental percentages; while Formaldehyde is number one on the list
it was not listed under the CERCLA priority list of hazardous substances (Friis,
2012) that was a requirement of the assignment, so; my choice was to focus on the
second most common hazardous substance in my community –Benzene.
Benzene is both a natural substance and a manmade
substance; highly flammable and slightly sweet smelling it is a colorless to light
yellow liquid when at room temperature that can evaporate easily into the
air. Naturally occurring Benzene is
found around volcanoes and during forest fires. Production of Benzene is mainly found as a
component in industries that make plastics, resins, dyes, synthetic fibers, and
pesticides and is ranked among the top twenty chemicals used in production in
the United States. Unfortunately in the
event of Benzene exposure there is no antidote for Benzene poisoning. The severity of Benzene poisoning is
dependent upon the quantity and length of exposure. Benzene exposure is dangerous due to how it
reacts in the human body. Benzene
attacks the cells in the body starting at the site of exposure and causes them
to stop working correctly. Blood cells are
the most susceptible to Benzene allowing for exposure to become systemic
causing issues with bone marrow production, a decrease in the number of red
blood cells, and a decrease in immune function.
These affects on the body can lead to anemia, prolonged bleeding time,
and cancers like leukemia.
Exposure to Benzene most often occurs through inhalation and
is found around gas stations, the emissions for motor vehicles, and industrial
complexes the biggest culprit of Benzene exposure comes from the inhalation of
cigarette smoke. Benzene levels can
often be found at higher levels more so indoors than outside. Indoor exposure to Benzene comes from the
glues and waxes used in furniture manufacturing, detergents, and paints. Because of its ease of exposure and toxicity
level, the Environmental Protection Agency has it listed “as a Hazardous Air Pollutant (HAP) under
the National Emissions Standard Hazardous Air Pollutants section of its Clean
Air Act” (OSHA).
The Occupational Safety
and Health Administration (OSHA) has strict guidelines for industry and workers
who handle Benzene on the job. Because
of Benzene’s ability to evaporate easily, job sites need to make precautions
available to prevent spills and splashes, provide employees with personal
protective equipment and respirators designed to protect against Benzene. Routine medical examinations of employees who
handle Benzene or work in areas with high concentration levels of Benzene are
recommended. For workplace preventative
exposure measures, employers are required by OSHA standards to provide personal
protective equipment from full body cover to air purifying respirators. The
respiratory protection standard for Benzene according to OSHA’s standard’s 29 CFR
1910.1028(g)(2)(i) and 29 CFR 1910-1028(g)(3)(i) state that “The employer must implement a
respiratory protection program in accordance with § 1910.134(b) through (d)
(except (d)(1)(iii), (d)(3)(iii)(b)(1) and (2)), and (f) through (m), which
covers each employee required by this section to use a respirator” (OSHA).
The health effects of
Benzene exposure are serious with its primary route of transmission occurring
through either inhalation or direct skin contact. Though Benzene is not readily absorbed
through the skin, there are instances that can speed up the process, such as;
open wounds and when in combination with other chemicals that are readily
absorbed. Health effects to the skin
include irritation at the sight and prolonged dermal exposure can cause drying,
scaling, and secondary infections.
Inhalation of Benzene when in high concentrations act as a stimulant to
the central nervous system and exposure is noted by changes in mood such as
nervous excitement, giddiness, periods of depression, drowsiness, and/or
fatigue. The individual may experience
sensations of tightness within the chest along with shortness of breath
followed by loss of consciousness. If the individual is not removed from the
area or if they experience a severe exposure their symptoms will progress to
tremors, convulsions, and respiratory paralysis which will ultimately result in
death within several hours from exposure.
Post exposure measures
are just as important as preventative measures.
Some measures are as simple as moving out of the exposure area
especially in the event of a Benzene leak.
Removing clothing that may have become contaminated with liquid Benzene,
cutting off those items of clothing that would require removal over the head so
as to avoid contaminating the exposed skin on the face and causing harm to the
eyes and nasal passages. Remove any
Benzene contamination to the skin with a thorough washing with lots of soap and
water, and rinsing eyes for a minimum of ten minutes if they are burning. Contaminated clothing and contacts (if worn)
need to be disposed of properly in a plastic bag using rubber gloves to avoid
further personal contamination. If an
individual is suspected of drinking or ingesting Benzene it is important that
they do not vomit and if they are unconscious not to do CPR, rather calling
paramedics is of the highest priority.
With Benzene such a
dangerous chemical, what actions are being taken to reduce exposure and
accumulation of Benzene particles in the air?
Through agencies like the Environmental Protection Agency (EPA) and laws
like the Clean Air Act, there are steps to reduce air toxicity and pollution
directed at some of the sources and causes for the reduction of Benzene levels
within the air we breathe. Benzene is
listed on the EPA’s list of mobile source air toxins for both on-road and
non-road vehicles/equipment. As of 2007,
the EPA has ruled that Benzene levels within gasoline and diesel need to be
reduced in order to reduce the amount of Benzene emitted in the form of
exhaust. Limiting or reducing one source
of Benzene from the air will greatly reduce exposure to the general populace. Minneapolis takes the EPA standard for
reduction of Benzene further with their anti-idling vehicle ordinance; limiting
the amount of time commercial and private vehicles can sit while simultaneously
saving fuel and reducing the Benzene levels in the air. This is important in that Minneapolis, like
most urban areas, can potentially have higher air toxin levels of many
different compounds that can be just as destructive to health as Benzene.
Reference:
Center for Disease
Control and Prevention. (2013). Emergency Preparedness and Response:
Environmental
Protection Agency. (2014). Overview: Pollutants and Programs: Mobile Source
Environmental
Protection Agency. (un). My Environment: 55417 zip code. epa.gov. Retrieved
Friis, R.H. (2012).
Essentials of Environmental Health (2nd edition). Chapter 6: CERCLA
Priority
List of Hazardous Substances; page 130.
Sudbury, MA: Jones & Bartlett Learning.
Occupational Safety
& Health Administration. (un). Medical Surveillance Guidelines for
Benzene. Regulations (Standards -29 CFR). US Department of Labor. Retrieved from: https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=10045
Occupational Safety
& Health Administration. (un). OSHA
Standards. US
Occupational Safety
& Health Administration. (un).
Safety and Health Topics: Benzene. US
Monday, April 28, 2014
An Epidemic of Obese Proportions
Abstract
Obesity is becoming one
of the most common diseases to date.
There is a lot of information stating why and how, but the current
methods of prevention and treatment are not slowing the rise in this epidemic. Through the use of medical texts and peer
reviewed journals, this paper looks at the reasoning behind the upward trend in
obesity in conjunction with epidemiologic observations, nutritional intake and
activity levels, metabolic syndromes, socio-demographics, and psychosocial
affects. Review of the current and
proposed means of prevention and treatment as well as the role that other
disease plays in obesity and vice versa.
An Epidemic of Obese Proportions
Obesity
is possibly one of the hardest issues to combat. It is not caused by a virus or bacteria and
cannot be cured with medication. Obesity
is defined as a condition when an individual having an excessive proportion of
their body weight as accumulated fat such that it poses a health risk. What are
the underlying causes that have made obesity such an overwhelming global
epidemic? What are the risks involved
for further disease brought on by obesity?
Obesity is a challenging health issue that has a multifaceted cause and
effect factor that needs to be understood in order for it to be treated and
prevented. Our behaviors and
socioeconomic outlook on ourselves and our place within society have dictated
our need for more –of everything- in order to feel full or fulfilled, yet the
changes we have made to our foods and activities has left us empty; if changes on
all levels –behavior, socioeconomic, psychological- are not made, the obesity
epidemic will continue to grow.
Behavioral causes of obesity
There
are many agreed-upon factors influencing why an individual becomes overweight
or obese (let alone the global population), but negative behavior choices are
at the top of the list. Some of these
behaviors are learned from parents, some are a part of the negative environment
we as a global society have created, and some are unknowingly induced at the
psychological level through the media, advertising industry, and the concept of
food security.
These
negative behaviors that perpetuate an obesogenic lifestyle include: eating
habits, sedentariness, and sociodemographics.
Eating habits are typically defined as the increased consumption of poor
yet highly energy-dense foods outside of the home. Sedentariness is a decrease in physical
activity such that it creates health risks. And sociodemographic variables of
gender, age, and education levels determine access to and understanding of food
choice, financial and health costs associated with negative health behaviors,
and food security that stipulates affordability, physicality, and social needs
of healthy foods versus cheaper energy-dense and fast food choices.
These behaviors combined with the increase in convenience
availability and the increased demand of conveniences, such as, transportation,
cooking, cleaning, and communication have only made these behaviors have become
a perceived social norm. While the
stigmas around being obese include stereotypes like being lazy or lacking
self-control we have created an environment for ourselves through our demands
for more convenience that have perpetuated the stereotypes into phenotypes.
Clinical Causes of obesity
Not
all obesity causes are the result of poor health behaviors. “There are over 600
genes, markers, and chromosomal regions identified as being associated with
human obesity phenotype” (Ulijaszek, 2007).
In the United States obesity is considered the most common nutritional
disorder costing more than $100 billion a year in health-related expenses. Research has shown that mutations at the
genetic level have been found to be associated with obesity; thus showing that
environmental factors that play roles in gene mutation have a greater potential
to become more prevalent with successive generations.
Most
clinical causes of obesity are termed secondary causes and can be brought about
by medications, other diseases, and psychosocial aspects. There are a number of medications that have
weight gain as a side effect. Thankfully,
for some of these medications, there are alternatives that offer either less
weight gain, no weight gain, or promote weight loss. These medications fall into the
pharmaceutical classes of psychiatric/neurologic, steroid hormones,
anti-diabetic agents, antihistamines, antihypertensive agents, and highly
active antiretroviral therapies. As for
obesity being a comorbid diagnosis of another underlying disease, the average
among obese individuals falls below 1%.
Those diseases that have a greater potential for causing obesity as a
secondary disease fall under endocrinopathies which include: Cushing’s
syndrome, hypothalamic damage, insulinoma, and hypothyroidism. Psychosocial aspects of obesity include:
sexual, physical, and emotional abuse –especially when it occurs in women or
during childhood or adolescence.
Society’s impact on obesity
Society’s
impact on obesity may not be very recognized or readily acknowledged. The move from agrarian to industrialized
life-styles and the implementation of the 7-day work week has changed not only
the access to physical activity and food but the structure of these same daily
activities. Combined with the increase in low cost transportation, the decline
of physical activity in highly industrialized nations these associations have
been well documented as being a part of the obesogenic societal creation. The spiral continues downward as the need to
reduce time constraints on daily living creates greater deficits in physical
activity. “Convenience in food is also
expressed in the emergence of fast food.
Eating at fast-food restaurants is positively associated with having
children, a high-fat diet, and high BMI, but negatively associated with
vegetable consumption and physical activity” (Ulijaszek, 2007).
Within
the United States the goal of improving test scores of standardized tests (No
Child Left Behind Act) has done little to impress upon our nation’s growing
children the value and need for physical activity. Physical education programs and sports
programs (along with programs in the arts) have had funding and time reduced,
if not cut altogether. With schools
held accountable for improved testing scores, many states developed rewards and
penalties for those schools that showed improvement and for those that
didn’t. As an unrecognized side effect,
schools and school districts reacted accordingly cutting time from those
activities and educational necessities like physical education, the arts, and
even recess which offered a chance of fresh air and sunshine if not some form
of physical activity, as a way to compensate for poor test scores. “In
a nationally representative sample, the presence of school accountability and
years of exposure to accountability laws significantly increase students’ BMI” (Schnider, 2013).
Thanks
to government subsidies unhealthy food has become abundant and inexpensive as
the costs of these products (sugar, corn, wheat, soybeans, and dairy) decrease
they become more readily available and easier to obtain while the cost of whole
foods (fruits and vegetables) have increased.
These cost differences affect most those in the poorer sectors
indicating that food security is one culprit in the obesity epidemic. It is no surprise that these same crops are
used in some of the most energy-dense foods containing high combinations of
sugar, fat, and salt and are some of the most accessible to all income levels.
Eating,
especially, has a historical social context.
When comparing those who eat alone versus those who eat in groups,
consumption of food in these social environments increases dramatically the
more individuals there are at the table.
“Obesity
spreads through social networks in adults.
Individuals ate 35% more when eating with one other person, 75% more
with three other people, and 96% more with a group of seven or more. Furthermore, an individual’s chance of
becoming obese increased by 57% if he or she had a friend who became obese and
37% if his or her spouse became obese.
These studies point to effects of environment and cultural influences on
obesity.”
(Swencionis, 2012)
Holidays, especially,
only perpetuate this group socialized eating setting and have been shown to
have become more food centered over the years and less religious centered over
the years.
Advertising of food is currently under scrutiny to see if
there is a deeper correlation between the number of advertisements an
individual sees regarding food per day and their risk of becoming obese. Marketing of food appears everywhere,
billboards, television, social media; sporting events (think the recent Winter
Olympics), mail flyers, magazines… the list goes on. It has been proven time and time again that
advertising works in the promotion of products as is shown by marketing
expenditures, and it has been shown that “industry marketing campaigns can even
counter the effect of health promotion messages” (Lesser, 2013). Surveys taken in middle and lower income
neighborhoods have shown that for every 10% increase within the neighborhood of
outdoor food advertising there is a 1% change, and in areas with 30% increase
in outdoor food advertising there is a 2.6% increase in the risk of becoming
obese.
Obesity’s dark side –disease caused
by obesity
The
epidemiology/pathophysiology behind obesity is anything but simple. Excess body weight is defined as a BMI of 25
to 28 for overweight and a BMI of 30 or more for obese and has long been
recognized in association to type 2 diabetes and an increased risk factor for
cardiovascular disease, but more recently through the literature review done by
the World Cancer Research Fund, there appears to be “convincing evidence that
body fatness is associated with an increased risk” of cancer (Renehan, 2008). Obesity has also been linked to an increased
likelihood of metabolic complications, insulin resistance, hypertension, dyslipidemia,
endocrine manifestations, obstructive sleep apnea, and gastrointestinal
disorders.
Obesity’s
havoc on the human body starts out small.
Metabolic complications occur when there is a greater concentration of
fat distribution in the upper body or in those with enlarged fat cells. Concentrations of fat like this result in the
release of free fatty acids and glycerol through the process of lipolysis,
which is regulated by insulin and catecholamines. This metabolic complication leads to insulin
resistance. Insulin in a healthy body
promotes the uptake of glucose, oxidation, and storage; when an individual
becomes insulin resistant the ability of these processes becomes reduced. Insulin resistance initially can lead to
hyperinsulinemia –a high risk factor in cardiovascular disease- and type 2
diabetes. Hypertension occurrence in
obesity is the result of decreased vascular relaxation caused by
hyperinsulinemia and its effects on renal sodium absorption. Dyslipidemia, like metabolic complications,
is associated with upper-body obesity and type 2 diabetes. The affects of dyslipidemia are an increase
in triglycerides, a decrease in high-density lipoprotein (the good
cholesterol), and high proportions of dense low-density lipoproteins (the bad
cholesterol).
Of
the abnormalities of endocrine function that occur in obese individuals one of
the most common abnormalities in obese women is polycystic ovarian
syndrome. The most common mechanical
complications brought on by being obese are an increased risk for lower
extremity degenerative joint disease and venous stasis which can be aggravated
by right heart failure. Obstructive
sleep apnea is more common in obese men and more common in women with the
upper-body obese phenotype. The cause is
due to the collapse of the upper airways during sleep due to the enlargement of
upper airway soft tissues and is associated with an increased risk of
hypertension, right heart failure, and sudden death. Obesity-caused gastrointestinal disorders are
associated with gastroesophageal reflux disease, gallstones, fatty liver, and
nonalcoholic steatohepatitis which can lead to cirrhosis of the liver and
death.
Obesity’s role in cancer is still being researched, but
the findings thus far have revealed connections between body fatness and an
increased risk of “oesophageal adenocarcinoma, and cancers of the pancreas,
colorectum, post-menopausal breast, endometrium and kidney, and evidence of a
probable association with risk of gall bladder cancer” (Renehan, 2008). Obesity-cancer caused mechanisms include
insulin resistance (insulin, C-peptides, insulin-like growth factors), sex
steroids (oestrogen and androgens), and adipokines (polypeptide hormones,
adipocytes, and leptin), though insulin resistance is considered to be at the
heart of the obesity-cancer associations.
Other biological obesity-related candidates include abnormal cytokine
production which is often seen in chronic inflammatory responses. These pro-inflammatory factors increase as
the fat mass increases. Pro-inflammatory
factors are secreted from adipocytes, meaning as the amount of fat accumulation
increases so does the amount of pro-inflammatory factors. Not only are these pro-inflammatory factors
recognized in connection with cancer, but also, in connection to the development
of insulin resistance, type 2 diabetes, and obesity-related
atherosclerosis.
When looking at the diseases caused by obesity it is easy
to see that there is a vicious cycle of cause and effect. As each stage in the cycle is obtained it
appears as though it is only easier for transition to the next stage of disease. Recognition of obesity’s dangerous health
affects is important at the earliest possible stage in order to make any
attempt to keep the cycle from going forward toward death.
Combating Obesity
According
to Callahan “Most of the 67 percent who are overweight or obese will remain so
for the rest of their lives” (2013); thus the first line of defense in the
fight against obesity lies in keeping children from the same fate. Programs similar to those against smoking are
proposed as possible weapons in the arsenal against obesity: taxation on
sugared drinks and unhealthy highly processed foods, reducing or even banning
advertising of unhealthy foods to children, posting nutritional information on
restaurant menus, and reducing the cost of healthy foods. But these proposals run into major barriers: marketing
practice and the potential impact on shareholder wealth. The World Health Organizations report on Diet
and Nutrition, as quoted by Ghani, state that the “the marketing practices
targeting children as ‘causative,’” allow for the potential targeting of
marketers for interventions (2007).
While proposals are good, test data have shown negative impacts that
reflect abnormal stock price reactions when companies are exposed as “obesity
related costs in marketing, consumer education, and increased regulation”
(Ghani, 2007). The forecasts for
shareholders potential losses make forcing changes in marketing and potential
legal implementation against companies who produce obesogenic-type foods and
products very difficult.
While
it has been clearly shown that negative environmental factors that influence
individuals to eat outside of the home has a high correlation to obesity, the
contrast exists for those who take a more conscious path in eating. Consumption of four or more meals per day,
eating whole foods and skim dairy products, trimming visible fat from meats or
choosing leaner meats, and avoidance of eating while otherwise distracted
(watching television) have proven to help with weight control. “Perceived barriers can have a negative
effect on commitment to a behavior; situational or environmental influences
affect commitment to and engagement in a given behavior; persons are more
likely to engage in a behavior if they have positive role modeling and support;
and that families, peers, and health care providers are important sources of
support for promoting a given behavior” (Moore, 2014; quoting Pender et al.,
2002).
Taking a threefold support concept of family, peers, and
health professionals it should be possible to come up with steps to promote
better behavior patterns while simultaneously recognizing the negative
behaviors which promote the obesogenic lifestyle in the first place. “Behavior condition therapy for obesity
consists of self-monitoring, stimulus control, and behavior modification. Self-monitoring is usually by diary. Stimulus
control consists of restricting eating locations, not engaging in other
activities while eating, restricting quantities, leaving the table soon after
finishing, shopping only from a list and restricting shopping to that list, and
making snack foods unavailable or difficult to obtain” (Swencionis, 2012).
Conclusion
Clearly,
obesity has become a disorder of convenience.
Acceptance of the global dependence upon the convenience of energy-dense
and highly accessible foods that have been proven to increase our
susceptibility to obesogenic living; acceptance of our dependence upon those
convenience making devices (cheap transportation, entertainment); and acceptance
of our psychosocial changes in our views on food and physical activity have
driven us down a dangerous path. Obvious
and not-so-obvious changes need to be made. Stopping the epidemic of obesity
will take the global effort of everyone and of many generations; but we need to
start now.
Reference
Callahan, D. (2013).
Obesity: Chasing an Elusive Epidemic. Hastings Center Report, 43(1), 34-
40.
DOI:10.1002/hast.114
Ghani, W. I., Childs,
N. M., & Szewczyk, S. H. (2007). Food Marketing Practices and Anti-
Obesity
Policy: Impact on Shareholder Wealth. Marketing
Management Journal, 17(1), 123-135.
Retrieved from: http://eds.b.ebscohost.com.lib.kaplan.edu/eds/pdfviewer/pdfviewer?sid=eb81aab8-fc67-43d0-b6b5-e378e0b8f6b7%40sessionmgr115&vid=4&hid=104
Goldman, L. and
Auseillo, D (ed). (2004). Cecil Textbook
of Medicine 22nd Edition.
Philadelphia,
PA: Saunders.
Lesser, L. I.,
Zimmerman, F. J., & Cohen, D. A. (2013). Outdoor advertising, obesity, and
soda
consumption:
a cross-sectional study. BMC Public
Health, 13(1), 1-7. DOI:10.1186/1471-2458-13-20
Mesas, A.; León-Muñoz,
L.; Guallar-Castillón, P.; Graciani, A.; Gutiérrez-Fisac, J.; López-
García,
E.; et al. (2012). Obesity-related eating behaviours in the adult population of
Spain, 2008-2010. Obesity Reviews: An
Official Journal of the International Association for the Study of Obesity, 13(10),
858-867. DOI:10.1111/j.1467-789X.2012.01005.x
Moore, M.M.; Robinson,
J.C.; Rachel, M.M.; and Boss, B.J. (2014). Barriers to Physical Activity
and
Healthy Diet Among Children Ages 6 Through 13 in a Mississippi Elementary School. Journal
of Pediatric Nursing, 29(2014), 74-82. DOI:10.1016/j.pedn.2013.08.010.
Renehan, A., Roberts,
D., & Dive, C. (2008). Obesity and Cancer: Pathophysiological and
Biological
Mechanisms. Archives of Physiology and
Biochemistry, 114(1), 71-83. doi:10.1080/13813450801954303
Schneider and Zhang.
(2013). School Accountability and
Youth Obesity: Can Physical
Education
Mandates Make a Difference? Educational
Research International, 2013(2013). DOI: 10.1155/2013/431979
Swencionis, C. and
Litman Randell, S. (2012). The
Psychology of Obesity. Abdominal
Imaging, 37(2012),
733-737. DOI:10.1007/s00261-012-9863-9.
Ulijaszek,
S.J. (2007). Obesity: a disorder of convenience. Obesity Reviews: An Official
Journal
of the International
Association for the Study of Obesity, 8(Suppl. 1), 183-187.
DOI: 10.1111/j.1467-789X.2007.00339.x
Friday, April 25, 2014
Tuesday, April 22, 2014
Quote of the Day
“In the spring, at the end of the day, you should smell like dirt.”
― Margaret Atwood, Bluebeard's Egg
― Margaret Atwood, Bluebeard's Egg
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