Cigarette Smoke Effect Photoshop

[Adriana Gowen]

Smokeeffects can be easy to create when you follow this tutorial on how to create a smoke Photoshop action. We'll use smoke brushes in Photoshop to create a unique Photoshop effect you can use to add smoke to photos.

To create a convincing Photoshop smoke effect, you'll need special smoke brushes. And, of course, you'll need a photo to work on. Here are the assets I'll be using in this tutorial on how to add smoke in Photoshop:

Create a snapshot of the whole image with Control-Shift-Alt-E. Add Gaussian Blur to it. Then take the selection from the middle mask and add it as a Layer Mask.

Now you know how to create a smoke effect in Photoshop, using the technique of Photoshop actions. Here's the finished result, and below you'll find even more examples of how you can make this awesome smoke Photoshop effect your own.

You've gone through the process of how to add smoke in Photoshop. However, you may not always have the time or interest to do it yourself. That's where the premium smoke Photoshop effects from Envato Elements come in.

By subscribing to Envato Elements for a low monthly fee, you get access to tons of high-quality creative digital assets, including Photoshop smoke effects and Photoshop smoke overlays. Here are a few premium smoke Photoshop effects, ready to download from Envato Elements.

With this action, you'll be able to add realistic, animated smoke clouds to your photos. All you need to do is to paint a selection and play the action twice. It's the best way to add smoke to photos without having to learn how to create smoke in Photoshop.

If you want to make your photo more magical, with this set of smoke effect Photoshop actions you'll be able to produce an effect of colorful smoke clouds surrounding your subject. Choose from 19 color options, and adjust the result as you see fit to put together smoking Photoshop effects.

Or maybe you're interested in creating a ghost-like effect? This action makes your subject look translucent, and the clouds of smoke give it an ethereal look. It's a very artistic smoke Photoshop effect that you can achieve with a single click, and without going through the process of how to add smoke in Photoshop.

If you want more control over the whole process, here you can find ten Photoshop smoke overlays that you can add manually, exactly the way you want. They're very simple to use and give an instant effect. Even if you know how to create smoke Photoshop actions, this is a great option to let your creativity out.

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Tobacco use is associated with an increased risk of hearing loss in older individuals, suggesting cigarette smoke (CS) exposure may target the peripheral auditory organs. However, the effects of CS exposure on general cochlear anatomy have not previously been explored. Here we compare control and chronic CS exposed cochleae from adult mice to assess changes in structure and cell survival. Two-photon imaging techniques, including the imaging of second harmonic generation (SHG) and two-photon excitation fluorescence (TPEF) from native molecules, were used to probe the whole cochlear organ for changes. We found evidence for fibrillar collagen accumulation in the spiral ganglion and organ of Corti, consistent with fibrosis. Quantitative TPEF indicated that basal CS-exposed spiral ganglion neurons experienced greater oxidative stress than control neurons, which was confirmed by histological staining for lipid peroxidation products. Cell counts confirmed that the CS-exposed spiral ganglion also contained fewer basal neurons. Taken together, these data support the premise that CS exposure induces oxidative stress in cochlear cells. They also indicate that two-photon techniques may screen cochlear tissues for oxidative stress.

Tobacco use correlates with an increased risk of high-frequency hearing loss in older individuals1. Since an estimated thirty-six million Americans smoke cigarettes2, this correlation confers a large social and economic burden. However, the origins of this correlation are unclear. In the United States, smokers are more likely to hail from poorer socioeconomic groups, who are at additional risk for hearing loss3. Moreover, individuals who accept the known health risks incurred through smoking may be less likely to protect their hearing from other sources of damage, including noise. These observations raise the possibility that smoking may not directly impact the cochlea, but rather correlate with other risk factors for hearing loss.

Burning tobacco initiates a complex chemistry of reactive organic molecules and free radicals, which are immediately inhaled into the lungs and sinuses of exposed individuals4. These molecules may access the cochlea through the bloodstream, or alternatively, via the Eustachian tube, which opens into the nasal part of the pharynx during swallowing5. One such component, nicotine, binds to nicotinic acetylcholine receptors (nAChR) present throughout the nervous system6, including the cochlea7. While the effects of CS exposure on inner ear cells have not been explored, there is epidemiological evidence that passive CS inhalation increases the likelihood of Eustachian tube dysfunction8. For endothelial cells and lung, CS exposure drives an inflammatory response as a consequence of oxidation9. Later stages of inflammation include cell death and destruction of the extracellular matrix (ECM, reviewed in10). The combination of apoptosis, inflammation, and ECM degradation causes alveolar enlargement and a loss of elasticity11. These destructive processes culminate into chronic obstructive pulmonary disease (COPD,12).

SHG/TPEF imaging has been used to quantify fibrosis in liver tissue17 and kidney tissue16, and assess cartilage degeneration36 and tumor progression31. Others have previously used SHG and TPEF imaging to investigate pathological changes to the cochlea. In one such study, intravital multiphoton microscopy was used to measure the volume of the scala media compartment in the apical turns of control and pendrin-deficient mice37. In another, little difference was observed between the SHG signals detected from the SG and basilar membranes of control and noise-exposed cochleae21. In contrast, we see significant divergence between CS-exposed and control tissues (Fig. 1). The altered levels of SHG signal observed here may also be compared to similar changes in chronic arthritis models38. We anticipate that this rapid, non-destructive, and powerful imaging technique shows great promise for future studies that screen for widespread changes in the cochlea.

Increased oxidative stress, particularly in the form of lipid peroxidation products, is observed in many tissues after CS exposure, such as the lung39. We similarly see a dramatic and widespread increase in lipid peroxidation products in SGN after CS exposure (Fig. 3). This result supports our quantitative TPEF analysis of oxidative stress (Fig. 2). TPEF appears to be somewhat less sensitive for oxidative stress compared to antibodies for lipid peroxidation (Fig. 3). Lipid peroxidation may be due to the presence of various free radicals in tobacco smoke4. Non-nicotinic compounds in cigarettes activate antioxidant response genes in endothelial cells, correlating with CS extract toxicity for brain microvasculature40. Microvascular pathology is also associated with different forms of hearing loss41. Further experiments will be needed to determine if CS exposure drives a microvascular pathology in the inner ear.

This study may be considered opportunistic. Most studies of disease or environmental exposure concentrate on a single organ system. For example, the mice used here were part of a larger cohort from an investigation of COPD development in the mouse lung after chronic CS exposure. We note that in humans, chronic CS exposure is associated with a broad range of health problems in addition to COPD. Hearing loss, for example, has been linked to smoking in multiple studies1,49,50,51. Thus, CS exposure via systemic oxidative stress may have repercussions on hearing loss while COPD/emphysema ensues. However, the mechanism of CS-induced hearing loss is not known. Prior to commencing this secondary analysis, we discussed aspects of the protocol that were applicable to hearing. As the CS- and air-exposed mice experienced the same levels of environmental noise and stress, with the sole difference being the presence of CS, we considered that a secondary study, on whether CS induces anatomical changes in the inner ear, would be interpretable. However, opportunistic studies are unfortunately limited in scope, as we were unable to perform functional studies to assess if CS-exposed mice have changes in their hearing thresholds50 or distortion product emissions49,52, as reported for humans.

Future experiments could further confirm and extend the findings reported here. Functional hearing studies on CS-exposed animals, including studies of noise damage and recovery, will further illuminate the effects of smoking on the auditory system. It would be interesting to use SEM to examine the cochlear surface for changes in ECM, for example. Cochlear stiffness could also be assayed through cochlear gel analysis53. One may also wish to investigate potential changes in cortical auditory regions, such as the MOC and LOC. We have not yet determined which component of CS drives the changes we report, whether it is nicotine, oxidizing radicals or some combination of the two. Nonetheless, this is the first study to analyze the anatomical effects of chronic CS inhalation on the cochlea in an animal model. Our findings support an interpretation that exposure to CS increases oxidative stress in the cochlea and correlates with a reduction in the numbers of high-frequency spiral ganglion neurons.

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