Dear Doctor: Just how unsafe is chromium-6, the chemical at the heart of the movie "Erin Brockovich"? I read that it's still in the water in some parts of the country. How is that possible? How do I find out about water quality in my area?

Dear Reader: While the characters and events in "Erin Brockovich" may have been embellished to serve the dramatic arc of the story, chromium-6, when present beyond certain concentrations, is as toxic as the film portrayed. Breathed in, it can cause lung cancer. Ingested, it has been linked to liver and kidney damage, serious reproductive problems, rashes and skin conditions, and developmental harm to infants and children.

Chromium is a metallic element that occurs naturally in soil, rocks, plants and volcanic dust. It is found in several forms, including chromium-3, an essential micronutrient that plays a role in the breakdown of fats, proteins and carbohydrates. Chromium-6, by contrast, is a toxic form of the element. Also known as hexavalent chromium, it's a byproduct of the natural chemical breakdown of chromium and is created in greater quantities through various industrial processes.

Both forms of chromium are used in applications such as chrome plating, making pigments and dyes, the manufacture of stainless steel, preserving wood and leather products, and, as depicted in "Erin Brockovich," in the treatment of water in cooling towers. Exposure to large amounts of any kind of chromium, which has numerous uses in manufacturing, has been known to cause respiratory problems like shortness of breath, wheezing, cough and even asthma.

When industrial users of chromium-6 fail to take proper precautions when they store or dispose of the chemical, leakage and runoff from the manufacturing process can pollute the groundwater. And while the EPA has set a limit on what it refers to as "total chromium," the sum of chromium-3 and the far more toxic chromium-6, at this time it has not set a limit solely for chromium-6. California, home to the landmark chromium-6 lawsuit at the heart of "Erin Brockovich," has placed a legal limit on chromium-6 concentrations in the water, but some activists believe the allowable levels remain too high.

You've posed an important question when you ask about how chromium-6 continues to enter our drinking water supply. But the answer is complex. Providing potable drinking water to a nation as vast and populous as the United States remains an ongoing challenge. Since the establishment of the Clean Water Act in 1972, health and safety standards have been set at the federal level. However, water is a regional resource. That means oversight of the tens of thousands of state, local and private water utilities that make sure our taps are flowing falls to a complex patchwork of regulatory agencies. As a result, water quality can vary greatly depending on where you live.

If you live in a community whose water system serves more than 100,000 people, it is required to post reports on water quality online. If you live in a smaller community, check with your local government agency to learn where and how to find reports regarding your specific provider. For more information, go to water.epa.gov/drink/index.cfm.

(Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles, CA, 90095. Owing to the volume of mail, personal replies cannot be provided.)

Dear Doctor: I'm a middle-aged woman on blood pressure medication, but recently heard that one type of this medication could raise the risk of pancreatic cancer. What type is that, and if it's mine, should I change?

Dear Reader: It's scary to think that a medication to improve your health could also cause disease. So let's take a closer look at the recent data from the Women's Health Initiative on the possible link between blood pressure medications and pancreatic cancer.

In the study, 145,551 postmenopausal women, ages 50 to 79, were asked about their use of anti-hypertensive medications. The women were followed on average for about 13.8 years, and 841 cases of pancreatic cancer were noted in that time. Women who had ever used calcium channel blockers (CCBs) for high blood pressure had a 33 percent increased risk of the cancer compared to those who had never used the drugs. Those who had used the drugs for three years or more had a 48 percent increased risk of pancreatic cancer compared to those who never used them.

Calcium channel blockers have been around for many years, with most of those used in the past being the short-acting variety. The authors found that women who had ever used the short-acting type had a 66 percent increased risk of pancreatic cancer, and those who had used them for three or more years had a 107 percent increased risk -- both as compared to women who had never used the drugs.

Keep in mind that most CCBs given today are the extended-release variety. When the authors looked at the extended-release CCBs, they found no association with pancreatic cancer. Nor did they find an association with any other medication for high blood pressure. At the time of this writing, the full article about the findings was not yet available, so it is difficult to know if confounding factors were involved, but the authors did say that they adjusted for obesity, diabetes, smoking and age.

The traditional short-acting CCBs are verapamil, diltiazem and nifedipine. As for why they might increase the risk of pancreatic cancer, chronic inflammation may play a role. The authors theorized that CCBs may block the release of a receptor needed to counter inflammation. In fact, in the 489 pancreatic cancer patients in whom levels of the receptor were measured, CCBs reduced the level of the receptor, thereby theoretically increasing the rate of pancreatic cancer.

While the preliminary data are concerning, they're not wholly definitive. If you're taking the short-acting verapamil, diltiazem or nifedipine, I would consider switching to an extended-release form of this medication. Although long-acting CCBs have not been associated with risk, you could also consider changing to an entirely different class of medication, such as an ACE inhibitor, an angiotensin receptor blocker, an alpha blocker, a diuretic or a beta blocker. Your doctor is the best person to decide which is the most appropriate choice.

And please note: The data was taken from postmenopausal women, so it may not be applicable to women who have not gone through menopause or to men.

(Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles, CA, 90095. Owing to the volume of mail, personal replies cannot be provided.)

Dear Doctor: I read that scientists are close to being able to "turn off" inflammation. What does that mean? And isn't that dangerous, since inflammation is a natural part of the immune system?

Dear Reader: The body's inflammation reaction is a double-edged sword. Most of the time we're grateful for the array of specialized white blood cells that rally to our defense. First to the scene of injury, illness and infection, they're specialists in detecting bacteria, viruses and other harmful organisms. They not only emit chemicals that destroy harmful invaders, they also cart away debris and rally the rest of the immune system to mount a robust response.

That's all great when things are working properly. But sometimes the body's inflammation response goes haywire. The same white blood cells that race to the rescue can be triggered by a case of mistaken identity and attack the body's own tissues. That's what's happening in autoimmune diseases like lupus, Crohn's disease or rheumatoid arthritis.

Certain conditions, like obesity, can rev up the inflammation process as well. That's because fat cells produce a class of small proteins known as cytokines, which are the same biochemicals that our white blood cells produce when they're on the attack. Those cytokines act as a 911 call to a host of other immune system cells, and thus encourage a state of ongoing inflammation. In addition to the autoimmune disorders we mentioned earlier, chronic inflammation has been linked to heart disease and certain cancers. And studies suggest that inflammation may have a hand in some diseases of the central nervous system as well.

All of which brings us back to the recent research that (we suspect) prompted your question. Among the cells that get involved in that initial immune response are white blood cells known as macrophages, which circulate throughout the tissues of the body. Now, a team of scientists from the United States, Ireland and the United Kingdom has identified a metabolic process that's able to get macrophages to stand down.

It turns out that a molecule known as itaconate, which is derived from glucose, acts as an "off" switch for macrophages. In a study published recently in the journal Nature, the researchers reported that the macrophages themselves can be instructed to make itaconate from glucose molecules. The presence of itaconate blocks the cascade of biochemical processes that add up to inflammation.

Specifically, a derivative of itaconate that can move in and out of the walls of our cells can actually decrease the production of cytokines, those small signaling proteins we were talking about earlier. The ability to control how macrophages produce and disperse cytokines would mean that certain types of inflammation could be controlled, or even stopped. The fact that it appears cytokines play a role in pain adds another intriguing layer of possibility to this discovery.

But before we celebrate the end of random inflammation, it's important to understand that at this point, the research has focused on mouse and human cells. The leap between the petri dish and the release of a targeted medication to control inflammation is a huge one.

(Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles, CA, 90095. Owing to the volume of mail, personal replies cannot be provided.)