Lead paint suit results in $2.1 million award

Jury awards millions to youth, who was poisoned by
lead paint as a toddler.

A Baltimore jury has awarded nearly $2.1 million to a 17-year-old city youth who was allegedly poisoned by lead paint in the 1990s when he was a toddler in an East Baltimore rental home.

The judgment against Elliot Dackman and the estates of Sandra and Bernard Dackman came recently in Baltimore Circuit Court, at the end of the weeklong trial of a lawsuit brought on behalf of Daquantay Robinson by his mother, Tiesha Robinson.

The jury verdict shows the long-running tide of litigation over the widespread use of lead-based paint in Baltimore's older rental housing has yet to ebb, according to Bruce Powell, the Robinsons' lawyer.

Though Maryland lawmakers enacted a law in 1994 meant to protect young tenants from lead-paint risks, Powell said, "Here we are; there are still a lot of cases."

Dozens of cases remain outstanding naming Elliott Dackman as a defendant, for example.

Daquantay Robinson had enough lead in his blood to be considered poisoned for more than 18 months while his family lived in a Darley Park home owned by the Dackman Co., Powell said.

According to documents submitted at trial, blood samples taken every six months and analyzed by Johns Hopkins medical laboratories repeatedly revealed what were then considered to be elevated levels of the toxic metal in the toddler.

Sandra Moses, the youth's grandmother, who testified at the trial, said she noticed flaking and chipping paint in the home when the family moved in just before Daquantay was born. She said she called the landlord to complain about it some time later.

"They didn't send anybody out to do any repairs, and I called several times" Moses, 50, recalled.

Subsequent testing after the lawsuit was filed found that while the home has since been substantially renovated, there are still surfaces there with lead paint on them, the family's lawyer said.

Frank F. Daily, who represented the defendants, declined to comment. Circuit Judge Alfred Nance presided over the trial.

Expert witnesses called for the family testified that the youth suffered permanent brain damage as a result of his exposure to lead, leading to learning and behavior problems.

Exposure to lead paint has
resulted in brain damage,
expert witnesses say.

Moses said he "has a hard time keeping up with the other students" in high school.

"Studies have consistently shown that exposure to lead paint, especially in children under the age of 6, can result in a lifetime of medical expenses and financial instability," Powell said in a statement announcing the verdict. "Although no monetary settlement can replace what has been taken from this child, we do feel vindicated when the responsible landlords are brought to justice in court."

It's unclear how much money will actually go to the plaintiff. The jury awarded $1.27 million in economic damages for lost earnings and $818,000 for pain and suffering, the family's lawyer said, but noneconomic damages are capped under state law at $545,000.

The landlord's insurance company also contends it's only liable for a fraction of the damages because it didn't cover the property the entire time he lived there, Powell said.

"There's going to have to be further litigation to get the victim paid," the Robinsons' lawyer predicted.

The award, coming 15 years or more after the youth's alleged exposure to toxic lead paint, highlights the price people continue to pay for Maryland's gradual, at times halting approach to dealing with the health hazards posed by the paint's widespread use in housing decades ago, said Ruth Ann Norton, president and CEO of the Green & Healthy Homes Initiative. The group, formerly known as the Coalition to End Childhood Lead Poisoning, has advocated for stronger lead-paint laws and regulations for decades.

The Darley Park home had been registered with the Maryland Department of the Environment before the Robinsons moved in, as the law required then for all rental units built before 1950. (That was the year lead-based paint was banned in Baltimore city out of concern for its health effects.) Jay Apperson, a state spokesman, said department records contain certification of "full risk reduction" at the property in 1996 before the Robinsons moved in, also as required.

Apperson could not say how the risk reduction was verified. But Norton said that for many years, the state allowed landlords to get by with a visual inspection to certify that lead-paint hazards had been properly dealt with. The only reliable way to check was to swipe window sills and other surfaces for lead-paint dust so fine it couldn't be seen, she said. Lawmakers began requiring lead dust tests in 2012.

Also, in the late 1990s, health standards had yet to require action in cases like Daquantay's. Since 1991, the U.S. Centers for Disease Control and Prevention had said anyone with blood-lead levels of 10 micrograms per deciliter or higher was considered poisoned. But Maryland health authorities were not expected to contact a poisoned child's family or inspect the home unless the level reached 15 micrograms per deciliter, noted MDE's Apperson. Daquantay's highest blood level was a notch below that threshold.

Since then, the CDC has declared that no amount of lead in blood is safe and lowered its "reference" level to 5 micrograms per deciliter.

"The rates this kid had are no longer considered to be a low-level poisoning," Norton said. "These are high."

With increasingly tighter regulations and stricter enforcement, the number of lead poisoned children in Maryland has declined dramatically since the late 1990s. The state is moving now to regulate lead paint in rental homes built between 1950 and 1978, when the federal government banned its sale for interior use. The state also is looking to enforce federal regulations requiring house painters and home improvement contractors take precautions when working even in owner-occupied homes.

"Over the past decade, there has been an increase in enforcement" of lead-paint laws and regulations, Norton said. "It's just regrettable it took so long to get those things in place for this particular family. One hopes we see less of this as we move forward with stronger enforcement and stronger laws."

Source: Baltimore Sun

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Aging brain affected by environmental exposures

The population of Americans aged 65 and older is expected to double between 2010 and 2050,1 and by mid-century the proportion of the human population made up of people over age 80 is projected to have quadrupled since 2000.

Seniors may be affected by poor IAQ and chemical
exposures earlier in life, researchers say.

So factors that affect this aging population are of increasing importance. Of particular concern are the neurological diseases and disorders typically associated with advanced age, among them Alzheimer’s and Parkinson’s diseases, dementia, and reduced cognitive function.

Investigators are studying the effects of not just present-day exposures and environmental influences such as physical and mental exercise, but also exposures that occurred much earlier in life, whose effects may only become apparent in old age.

It was long assumed that “once the brain received its allotted quota of nerve cells, its destiny was frozen. After that, the passage of time eroded our allotment steadily and irrevocably,” as professor emeritus Bernard Weiss of the University of Rochester School of Medicine and Dentistry wrote in 2007.3

Now, however, there is increasing evidence that the brain is capable of generating new neurons and other functional brain cells even during advanced age. There is also evidence that the older brain can respond quickly and positively to external influences such as physical exercise and intellectual stimulation.

This is prompting considerable interest in developing strategies for protecting and enhancing neurological function in the elderly.

The two most vulnerable periods for the brain, Weiss says, are early in life, when the organ is first developing, and later in life, when the body’s defenses and compensatory mechanisms begin to falter.

There is a large and growing body of evidence indicating these two vulnerable life stages can be linked when damage incurred during early development contributes to health disorders that may not become apparent until later in life.

Weiss also notes that declining defense mechanisms may magnify vulnerability to contemporary environmental exposures.

He says that when older adults experience cognitive problems, diagnoses rarely consider the possibility that environmental chemical exposure may be involved, simply because questions about such exposures are typically not asked as part of clinical intake.

Over the past 30 years, Weiss says, research attention has focused primarily on environmental influences on early developmental stages. Far less extensively researched, but a subject of increasing interest, are environmental chemical exposures that can affect the health of the aging brain.

Neurotoxic agents

In the past 10 years, however, a number of studies have looked at the effects of chronic low-level lead exposure on adult humans’ cognitive abilities. The findings of such studies suggest that lead that has accumulated in bones can be mobilized over time as part of the aging process, resulting in exposures that adversely affect adults’ cognitive skills later in life.

Other metals may adversely affect neurological function in later life by either acting directly on the brain or adversely impacting other organs or hormones that maintain healthy neurological function.

For example, cadmium can cause kidney disease, which is associated with cognitive problems. Like lead, cadmium is stored in the body, primarily in the kidneys and liver but also in joints and other tissues, where it has a biological half-time of decades.

Similarly, lead and mercury have been associated with liver disease, which itself is associated with adverse neurological health effects, including a condition that produces a type of neuronal plaque associated with Alzheimer’s disease.

Chemical exposures that adversely affect kidney and liver function can also hamper the body’s ability to detoxify and excrete environmental toxicants, thus letting them remain in the body—an effect that may be particularly problematic in advanced age when a body’s defense mechanisms are in decline.

There is evidence connecting certain metals (e.g., lead, manganese), pesticides (e.g., paraquat, maneb), and solvents (e.g., toluene, trichloroethylene) with neurological 
symptoms characteristic of Parkinson’s disease. Many of the exposures studied have been occupational, and some were acute, rather than lower-level and chronic. Much more extensive research is needed to determine the precise role environmental exposures to these agents may play in prompting Parkinson’s disease.

More substantial evidence links various solvent exposures to other neurological conditions, including cognitive impairments, neuropathy, and what is sometimes called “pseudodementia,” when temporary neurological dysfunction produces symptoms similar to those of dementia.

Organic solvents, including toluene, have also been found to impair color vision, while other solvent exposures have been linked to hearing loss, particularly when combined with noise exposure.

Such exposures have been primarily studied when they occur occupationally, but some epidemiological studies suggest there is also potential for adverse effects from ambient environmental exposures.

Solvent and pesticide exposures have
been linked to neurological disorders.

These solvent and pesticide exposures can, of course, occur at any age. But because the neurological disorders with which they are linked mirror those associated with motor and sensory-function declines of aging, they can be mistaken in diagnosis for the effects of aging or diseases of old age like Parkinson’s and Alzheimer’s diseases.

It also appears that long-term non-acute exposures to solvents and pesticides can affect verbal memory, attention, and spatial skills, with effects that may not become apparent until later in life, when they, too, might be confused with or compounded by aging-related conditions.

More subtle environmental exposures are also thought to be implicated in neurological health effects that can manifest later in life. These include exposures to chemicals that may disrupt the normal function of hormones involved in regulating neurological health, chief among them thyroid hormones.

Hormones are intimately involved with neurological function; a normal brain can’t develop without healthy thyroid hormone function, and the fetal brain is extremely receptive to thyroid hormone.

When environmental factors affect thyroid and other hormones, the result can be health effects associated with conditions that impair neurological function.

For example, there is evidence that exposure to persistent organic pollutants including dioxins and certain polychlorinated biphenyls, halogenated flame retardants, and pesticides can produce hormonally mediated effects that promote obesity and diabetes, which increase risk for vascular health problems.

There is also evidence that exposures to some of these same compounds may directly increase risk for hypertension and cardiovascular disease.

These cardiovascular conditions can, in turn, cause less dramatic neurovascular effects that sometimes result in memory loss, or what’s called “vascular dementia,” when reduced blood flow to the brain deprives brain cells of oxygen and causes the equivalent of small strokes.

Evidence of similar effects has been reported for exposure to chemicals that are pervasive due to widespread use but are not environmentally persistent.

Among these is bisphenol A (BPA).

Laura Vandenberg, an assistant professor of environmental health studies at the University of Massachusetts Amherst, explains that numerous animal studies indicate early-life exposure to BPA can produce health effects characteristic of metabolic syndrome.

Individuals with metabolic syndrome are at increased risk for hypertension, with its risk for adverse neurological effects. It is also often hard to exercise for those who are overweight or obese or who have cardiovascular disease or diabetes. Yet aerobic exercise in later life appears to be an essential component of maintaining, if not also enhancing, brain function in older age.

Protective Factors

There is now substantial research investigating how physical activity and exercise affect brain function. This is also the area of research where it is perhaps the easiest to make direct comparisons between animal experiments and human studies.

One focus is to understand the mechanisms by which exercise protects and restores the brain.

Of particular interest is learning how physical exercise increases the production of new neurons, and how that may enhance performance of certain memory functions. Functions of interest include what’s called “relational binding”—for example, remembering the name of a person you recently met and where you met that person.

Physical exercise also appears to enhance “visual pattern separation,” which enables you to distinguish and remember different patterns—a process that increases memory accuracy.

Source: Environmental Health Perspectives

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Fathers' solvent exposure linked to cancer in children

Parents' exposure to chemicals such as benzene, toluene and
TCE could be linked to brain tumors in their children.

Brain tumors in children could have as much to do with the father's occupational exposure to solvents as they have to do with the mother's, a new Australian study has found.

The study, published in the British Journal of Cancer, has found a link between parents' exposure to chemicals such as benzene, toluene, and trichloroethylene and brain tumors in their children.

Lead author Dr Susan Peters, occupational epidemiologist at the University of Western Australia, says while brain tumors are relatively rare they are a major cause of cancer death among children, and the causes are largely unknown.

"Because most of the cases occur before age five, the question is what are the risk factors because there are some genetic syndromes that are known to cause brain tumors but only in less than five per cent of cases," says Peters.

"The children are pretty young, [so] it could be that some of the parental exposures before or during pregnancy may be a cause."

The new study surveyed nearly 306 cases of parents of children up to 14 years old with brain tumors, which were diagnosed between 2005 - 2010 in Australia.

The researchers compared the parents' occupational exposures to solvents with those of 950 parents whose children did not have brain tumors.

The findings suggest that fathers working in jobs where they are regularly exposed to benzene in the year before their child is conceived are more than twice as likely to have that child develop a brain tumor.

Women working in occupations that expose them to a class of compounds called chlorinated solvents -- found in degreasers, cleaning solutions, paint thinners, pesticides and resins -- at any time in their lives also have a much higher risk of their child developing a brain tumor.

Building on previous studies

While brain tumors in children are relatively rare, previous studies have suggested a link between parental occupation and childhood brain tumors, finding parents working in industries such as the chemical and petroleum industries, car-related jobs, and jobs with regular exposure to paint, have a higher risk of their children developing brain tumors.

Peters says a previous study in rats also found that toluene -- found in petrol, paints, and inks -- had an effect on sperm cells, which points to a possible explanation for the link in humans.

Commenting on the study, Emeritus Professor Michael R. Moore, vice president of the Australasian College of Toxicology and Risk Assessment, says the data shows paternal exposure was a key issue.

"This is the children being directly affected by the father and the father's exposure is taking place prior to the children being conceived," says Moore.

"Parents who are thinking of having children should be thinking about not just what's happening with the mums but also with the dads."

Peters stressed that the study only involved relatively small numbers of cases, and it was still too early to say whether solvent exposure was the cause of childhood brain tumors.

However she said these solvents were associated with a range of other effects so exposure should be kept as low as possible anyway.

Source: ABC

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Males may be weaker sex when it comes to environmental pollutants

Men are more affected than women
by chemical exposures, studies show.

Contrary to cultural assumptions that boys are stronger and sturdier, basic biological weaknesses are built into the male of our species.

These frailties leave them more vulnerable than girls to life’s hazards, including environmental pollutants such as insecticides, lead and plasticizers that target their brains or hormones.

Several studies suggest that boys are harmed in some ways by these chemical exposures that girls are not.

Mother Nature has always acknowledged and compensated for the fragility and loss of boys by arranging for more of them: 106 male births to 100 female newborns over the course of human history. (Humans are not unique in this setup: Male piglets, as an example, are conceived in greater proportion to compensate for being more likely than female piglets to die before birth.)

But in recent decades, from the United States to Japan, from Canada to northern Europe, wherever researchers have looked, the rate of male newborns has declined. Examining U. S. records of births for the years between 1970 and 1990, they found 1.7 fewer boys per 1,000 than in decades and centuries past; Japan’s loss in the same decades was 3.7 boys.

Boys are also more than two-thirds more likely than girls to be born prematurely – before the 37th week of pregnancy. And, despite advances in public health, boys in the 1970s faced a 30 percent higher chance of death by their first birthday than girls; in contrast, back in the 1750s, they were 10 per cent more likely than girls to die so early in their lives.

The nine-month transformation from a few cells to an infant is a time of great vulnerability. Many chronic illnesses are seeded in the womb.

Once they make it to childhood, boys face other challenges. They are more prone to a range of neurological disorders. Autism is notoriously higher among boys than girls: now nearly five times more likely, as tallied by the U.S. Centers for Disease Control and Prevention.

They are more susceptible than girls to damage from very low-level exposure to lead. Yet another problem: Boys also suffer from asthma at  higher rates. There’s also a stronger link between air pollution and autism in boys.

Why do boys face such a burden of physical challenges?

The answer is that the male’s problems start in the womb: from his more complicated fetal development, to his genetic makeup, to how his hormones work.

In our species, the female is the default gender, the basic simpler model: Humans start out in the womb with female features (that’s why males have nipples). It takes a greater number of cell divisions to make a male; with each comes the greater risk of an error as well as the greater vulnerability to a hit from pollutants.

Females have a stronger immune system because they are packed with estrogen, a hormone that counteracts the antioxidant process.

If the balance of hormones is out of whack in males, what made that happen? Researchers are coming up with some clues, among them:

• Prenatal exposure to chemicals such as insecticide chlorpyrifos
• Pregnant mothers' exposure to phthalates – used in making some vinyl products and toys as well as some personal care products 
• Exposure to bisphenol A, an estrogenic substance used to make polycarbonate plastics as well as some thermal receipts and the linings of food and beverage cans

Some of these chemicals act like fake estrogens, others like fake testosterone, but both types seem to disrupt normal development. Animal tests show that a dose of these chemicals inflict the most damage when it hits a fetus. And, because of their biological vulnerabilities, it’s boys who may experience the most effects.

While not forgoing the push for fairness and equality, it seems wise to accept the scientific reality of male weaknesses. This likely won’t mean the end of men, but their vulnerability to environmental contaminants and diseases could have serious ramifications for the future of the entire human race unless we find ways to protect them from harm.

Alice Shabecoff is the coauthor with her husband, Philip Shabecoff, of Poisoned for Profit: How Toxins Are Making Our Children Chronically Ill, Random House 2008, Chelsea Green, 2010.

Source: Environmental Health News

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Chemical exposure and brain development: Researchers set to study effects

EPA awards more than $3 million to researchers

The goal of the studies is to improve
chemical safety: EPA

The U.S. Environmental Protection Agency (EPA) announced over $3 million in grants to research institutions to better understand how chemicals interact with biological processes and how these interactions may lead to altered brain development.

The studies are focused on improving EPA’s ability to predict the potential health effects of chemical exposures.

“This research will transform our understanding of how exposure to chemicals during sensitive lifestages affects the development of the brain,” said Lek Kadeli, acting assistant administrator for EPA’s Office of Research and Development.

“By better predicting whether chemicals have the potential to impact health and human development, these grants will not only advance the science necessary to improve chemical safety but protect the well being and futures of children in this nation.”

These grants focus on developing better adverse outcome pathways (AOPs), which are models that predict the connection between exposures and the chain of events that lead to an unwanted health effect.

AOPs combine vast amounts of data from different sources to depict the complex interactions of chemicals with biological processes, and then extend this information to explain an adverse health effect.

EPA expects to use the knowledge gained from this research to develop efficient and cost-effective models to better predict if and how exposure to environmental chemicals may lead to developmental neurotoxicity.

Recipients of EPA’s funding for developmental neurotoxicity adverse outcome pathway research include:

1. North Carolina State University, Raleigh, N.C.
2. The University of Georgia, Athens, Ga.
3. University of California, Davis, Calif.
4. Sanford-Burnham Medical Research Institute, La Jolla, Calif.

These awards are advancing the science and technological capability to model and predict how chemicals behave when they come into contact with biological systems.

This improved understanding supports the Agency’s mission of protecting human health and the environment and amplifies the impact of its chemical safety research efforts.

EPA’s chemical safety research is accelerating the pace of chemical screening, helping to protect vulnerable populations and species, developing solutions for more sustainable chemicals and using computational science to understand the relationship between chemical exposures and health outcomes.

Source: EPA

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Better air reduces death and disability rates: Study

Death and disability from air pollution down 35 percent in the U.S.

Air pollution affects hospital admissions,
mortality rates and cardiovascular disease,
research has shown.

A study by BYU professor Arden Pope concludes that improvements in U.S. air quality since 1990 have sparked a 35 percent reduction in deaths and disability specifically attributable to air pollution. Pope was a member of a large research team who co-authored the study for the Journal of the American Medical Association.

"Some of the best news relative to the air pollution research over the last few years is the evidence that our reducing air pollution in the United States has resulted in measurable improvements in life expectancy and public health," said Pope in a press release.

It's no coincidence that 1990 is a point of reference in air quality research. In the late '80s, a steel mill in Utah Valley shut down for one year due to a labor strike. Pope spotted a research opportunity that found big problems caused by small particles floating in the air. Known as "particulate matter," this kind of pollution is produced by combustion of car engines, power plants and steel mills.

Air pollution impacts lungs, heart and brain

Pope and other scholars found in successive studies that dirty air impacted hospital admissions, mortality rates, and cardiovascular disease – including the risk of heart attacks.

"One of the biggest surprises of this research was that air pollution contributed to cardiovascular disease and not just respiratory disease," Pope said. "In fact, we're learning that air pollution not only impacts our lungs but it impacts our heart and our brain."

The research caught the attention of scientists and regulators, which lead to automobile emissions standards and cleaner manufacturing processes.

Now a world-renowned expert on the topic, Pope was asked this year to evaluate the credibility of an intriguing study on China's air quality by scientists at MIT, Peking University, Tsinghua University and Hebrew University of Jerusalem. Editors of the Proceedings of the National Academies of Science invited Pope to write a commentary that accompanied a research paper on China's Huai River policy.

The Huai River runs west to east and is regarded as the geographical dividing line between northern and southern China. In winter, the Chinese government provides free coal to residents north of the river to heat their homes.

In denying coal to people who live south of the river, the Chinese government actually did them a favor. The researchers found that air pollution is 55 percent lower on the south side. They also estimated that life expectancy was five years lower on the north side because of the extra air pollution.

"While their results tend to be a bit higher than what we'd expect based on the rest of the literature, it's still roughly consistent with what we would expect based on the other studies that we've been doing," Pope said.

Source: Brigham Young University 

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